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Volume 33,2023 Issue 9

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Research progress in the regulation of glutamate in traditional Chinese medicine in the treatment of depression

li chao

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Glutamate is a major excitatory neurotransmitter in the central nervous system and a potential neurotoxin. During the development of depression, there is an increase in glutamate concentration in the hippocampus, and when glutamate accumulates, it will cause serious damage to neurons and brain tissue, aggravating the depressive state. Therefore, glutamate accumulation may be an important mechanism for depression. Astrocytes, glutamate transporters and glutamate receptors play important regulatory roles in the concentration of glutamate. This article reviews the mechanism of action of traditional Chinese medicine therapy on the treatment of depression by regulating astrocytes, glutamate transporters, and glutamate receptors, and provides new ideas for exploring the treatment of depression by traditional Chinese medicine.
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To explore cognitive differences among dogs with different sociability

song meng yu, guo yi jun, zhao xue rong, bai jing, zhou zi juan, wang jing yu

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Objective:Exploring whether there are differences in the cognitive abilities of socially different Labradors. Methods:The Dog Mentality Assessment (DMA) test created by the Swedish Working Dog Association was modified to use 12 behavioral variables from five subtests of the DMA test: Social contact, Play I, Distance-play, Ghosts and Play II to assess the sociability of the dogs. According to the scoring criteria,49 Labradors provided by The China Guide Dog Training Centre In Da Lian was scored on the social behavioral variables, which were classified into high (n=15) and low (n=34) sociability groups using cluster analysis. A new system for testing canine cognitive ability was developed based on Bray et al.'s Dog Cognitive Development Battery (DCDB), which tests different domains of cognitive ability such as social cue use, unsolvable task, inhibitory control, cognitive flexibility, working memory and multi-step problem solving task, and the dogs' behavioral performance and duration of the test were recorded. Statistical analysis was performed to determine whether there were differences in the cognitive abilities of socially diverse dogs. Results:Dogs in the high and low social subgroups differed significantly on behavioral variables in the unsolvable task, the inhibitory control test and the multi-step problem solving task. In the unsolvable task, dogs in the high social grouping average looked at people time for significantly longer than dogs in the low social grouping (P=0.008) and average looked at people for significantly less latency time than dogs in the low social grouping (P=0.0001). In the inhibitory control, dogs in the high social group chose correctly significantly more than dogs in the low social group (P=0.034) and chose for significantly less time than dogs in the low social group (P=0.039). In the multi-step problem solving task, dogs in the high social group successful completion number of stakes significantly higher than dogs in the low social group (P=0.044); the percentage of operation pale time was significantly lower than dogs in the low social group (P=0.05); the average latency time to solve bone task was significantly higher than dogs in the low social group (P=0.037); and the percentage of operation bone time was significantly lower than dogs in the low social group ( P=0.038). On tests involving manipulable apparatus, dogs in the high social group spent more time looking at people than dogs in the low social group and less time manipulating the apparatus than dogs in the low subgroup, but there were no statistically significant differences (P>0.05). Conclusions:High sociability labradors showed greater cognitive ability,they were more able to suppress impulses during the test, were more able to complete multi-step problem solving task and were more inclined to change strategies to seek new cues from people rather than obsessing over manipulating the apparatus when they were unable to solve a problem.
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Construction of a prognostic risk marker of colon adenocarcinoma based on weighted gene co-expression network and its clinical significance

liyihui

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Objective Due to the poor prognosis of colon adenocarcinoma (COAD) patients, it is necessary to screen prognosis-related genes in COAD and establish a new prognostic risk assessment model. Methods COAD-related data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were used as the training set and the validation set, respectively. Weighted gene co-expression network analysis (WGCNA)， Cox regression model and Least Absolute Selection and Shrinkage Operator (LASSO) regression analysis were used to screen prognosis-related genes of COAD and construct a prognostic model. Receiver Operating Characteristic (ROC) curve was combined with survival curve to verify the accuracy of the model, and a nomogram was established. The patients were divided into two groups according to the median value of risk score. The immune cell proportion score (IPS) was used to evaluate the immunotherapy response of the two groups. Results A total of 15 feature genes were screened. The area under the ROC curve (AUC) in the predictive model of COAD patients was >0.6, and the survival rate of high-risk group was significantly lower than that of low-risk group (P<0.05, suggesting good distinguishing ability for high- and low-risk COAD patients. Patients in the low-risk group had a higher IPS (P=0.026), indicating a better response to immunotherapy. Conclusions The model developed for COAD in this study has a good ability to predict the survival of people at high and low risk of COAD.
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Quality Evaluation for Animal Studies on Acupuncture for Glaucoma

lijiaxian, lianglina, 李亚敏, xukai, huangziyang, lixiaoyu, jinyu, zhouwei

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Objective To evaluate the quality of animal studies on acupuncture for glaucoma by the SYRCLE’s risk of bias tool, ARRIVE 2.0 guidelines and GSPC checklist. Methods Databases of CNKI, VIP, Wanfang, Sinomed, PubMed, Web of Science, Embase, and Cochrane Library were conducted to find animal research articles on acupuncture for glaucoma. Risk of bias was assessed for included studies using the SYRCLE’s tool, and the reporting quality was evaluated using the ARRIVE 2.0 guidelines and GSPC checklist, statistical analysis was performed by Excel and SPSS software. Results Thirty articles met the inclusion/exclusion criteria and were included in the final analysis. 6 of the 10 items of the SYRCLE’s tool had a low-risk rate of <50%, and the non-low-risk items focused on selectivity bias, implementation bias, and measurement bias. 12 of the 22 essential sub-items of the ARRIVE 2.0 guidelines had a low-risk rate of <50%; 9 of the 16 recommended sub-items had a low-risk rate of <50%; 12 of the 19 subentries of the GSPC list had a low-risk rate of <50%, and randomization, blinding, thical statement, housing and husbandry, animal care and monitoring, protocol registration were non-low-risk items in the ARRIVE 2.0 guidelines and GSPC list. Conclusion The quality of methodology and experimental reportings in animal studies on acupuncture for glaucoma are generally low, and the descriptions of several items are not yet complete, which affects the readers' judgment on whether the animal studies can be further translated into clinical studies. It is advised to further promote the SYRCLE’s tool and reporting guidelines for animal experiments, to enhance the design, performance, and reporting of animal experiments, ensure the reproducibility of experiments and results, and provide reliable evidence for the translation of results to the clinic.
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miR-181a-5p overexpression in the small intestine in a mouse model of subcutaneous transplantation of oral cancer

wuxuehai

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[Abstarct] Objective By detecting changes in metabolites and metabolic pathways in the small intestine of mice with subcutaneous transplantation of oral cancer, the effects of overexpression of miR-181a-5p on metabolites and metabolites in the small intestine of mice with subcutaneous transplantation of oral cancer were analyzed. Methodes Three groups existed in the experiment: the Control group, the Negative control group, and the Over expression of miR-181a-5p group in the experimental group. To construct a subcutaneous transplantation tumor mouse model of oral cancer, different groups of treated cell suspensions were subcutaneously injected into the right point and upper location of the groin of M-NSG severely immunodeficient female mice. The pathogenic changes in each group were identified while additionally following the changes in the mice's body weight and small intestinal tissues using HE staining. By using tandem Orbitrap mass spectrometry and ultra-high performance liquid chromatography-tandem time-of-flight mass spectrometry, the metabolites in the small intestine of mice in the NC group, OE group, and Control group have been detected. By pre-analyzing the original data and quality rating sample data, XCMS was able to assess which metabolites were different between the Control group and NC group and between NC group and OE group. To establish the unique metabolic pathways, KEGG enrichment analysis was used. Results A total of 170 distinct metabolites were found in the small intestinal tissues of the Control and NC groups. Choline metabolism, alanine, aspartate, and glutamate metabolism, GABA synaptic metabolism, glycerophospholipid metabolism, cAMP signaling route, cancer center carbon metabolism, and niacin and niacin amine metabolic pathways are important signaling pathways for metabolite enrichment. In the NC group, 16 distinct metabolites with VIP values larger than 2 were found in the small intestine of mice compared to the OE group that overexpressed miR-181a-5p. Glycerin phosphoylcholine, palmitic acid, 3-hydroxybutyryl carnitine, -hydroxybutyric acid, etc. are example of the metabolites which significantly vary. The primary raised metabolism path is the one for choline. Conclusions Mice's small intestine suffered slight changes as a result of subcutaneous transplantation of oral cancer, with the greatest effect in the metabolites critical in energy metabolism. The choline metabolic path was the pathway that selected absolutely metabolites in the small intestine of mice with the subcutaneous grafts of oral cancer.
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The effect of cobalt dichloride regulating inflammatory response and insulin resistance in 3T3-L1 adipocytes based on HIF-1α/ autophagy pathway

yuexinxin, Fu Yang, Li Yi Rang, Yin xiao yan, Yu Fei, Fu quan wei

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Objective: To investigate the effect of hypoxia inducer cobalt chloride (CoCl2) on autophagy in 3T3-L1 adipocytes. Methods: 3T3-L1 adipocytes were cultured and induced to become mature adipocytes. CoCl2 was used as an inducer of hypoxia in vitro. Mature adipocytes were divided into control group, CoCl2 intervention group with different concentrations and different time. According to the above results, 150μmol/L cobalt chloride was selected to intervene adipocytes for 0h,12h,24h and 48h, respectively. Then the cells were collected for related tests. MTT assay was used to detect cell survival in each group. The expressions of HIF-1α, autophagy-related protein LC3Ⅱ, Beclin 1 and glucose transporter Glut-1 were analyzed by Western blot. The level of autophagy activity was detected by immunofluorescence.The levels of TNF-α and IL-6 in the supernatants of adipocytes were measured by ELISA. Results: The survival rate of adipocytes was decreased after treatment with 150μmol/L CoCl2 for 24 hours. The expression levels of HIF-1α, LC3-Ⅱ, Beclin 1 and Glut-1 proteins were significantly increased in 24h. Autophagy activity level was significantly increased in 24h. The secretion levels of inflammatory cytokines TNF-α and IL-6 were not significantly increased in 24h. Conclusion: Autophagy can be moderately activated by 150μmol/L CoCl2 intervention in adipocytes for 24 hours. The activation of autophagy can be activated in a HIF-1α-dependent manner, which plays a role in protecting adipocytes from inflammatory damage and improving insulin resistance.
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Progress in microglia-astrocyte interactions and their mediated neuroinflammation in Alzheimer's disease

HU Xin, WANG Qian, ZHANG Chen-xi, ZHENG Hui-hui, LI Peng-yang, ZHAO Hong-ye, DENG Feng-chun

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Alzheimer's disease (AD) is an aggressive neurodegenerative disease whose pathogenesis is hitherto unknown. Neuroinflammation is a chronic inflammatory response in the central nervous system (CNS) activated by microglia and astrocytes that is difficult to subside autonomously and is associated with multiple inflammatory factors and the blood-brain barrier (BBB). Recent studies have shown that neuroinflammation has become the third major pathological feature in AD after β-amyloid (Aβ) deposition and neurogenic fiber tangles (NFTs). In this paper, we summarize and analyze microglia and astrocytes and their interaction, and organize and discuss the role of microglia-astrocyte interaction in neuroinflammation and AD. In order to provide a reference for the involvement of microglia and astrocytes in the pathological alterations of neuroinflammation in AD.
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Research progress of miRNA in neuroprotection of ischemic stroke

lihongyu, lanrui

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Ischemic stroke is a cerebrovascular disease with high disability and mortality, and can be life-threatening in severe cases, which has a heavy social and economic burden worldwide. The etiology and pathological process of ischemic stroke are mediated by a variety of molecular processes, and some of these molecular mechanisms are dynamically regulated after transcription. Increasing evidence has shown that Micro-ribonucleic-acid (miRNA), as an important mediator of post-transcriptional gene silencing, plays a crucial role in gene expression and the pathological process of ischemic stroke. In this review, we present the neuroprotective effects of mirnas in different mechanisms of ischemic stroke. Since the promotion or inhibition of miRNA expression through specific drug and non-drug therapy may be beneficial to the recovery of ischemic stroke, the clinical diagnosis and treatment of miRNA in ischemic stroke are also discussed in detail in this paper, aiming to provide a certain reference for clinical and basic research in this field.
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Research progress on the effect of miRNAs on liver metastasis of digestive system tumors

Yangsiqi, jinming, zouqinling

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Liver is the most common organ that tumors spread to, and expression of miRNA is very important in the process of liver metastasis. In this study, research progress of related miRNAs in regulating liver metastases from digestive system malignant tumors was collated and analyzed. Through searching related literature, this paper provides an introduction to the role of miRNAs in liver metastasis of colorectal cancer, gastric cancer, pancreatic cancer and gallbladder cancer, which helps with the diagnosis, treatment and research of tumor liver metastasis.
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Establishment of chronic alcoholic brain injury model in mice

Cai Yu

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【Abstract】 Objective To establish an effective and reliable chronic alcoholic brain injury model in mice. Methods C57BL/6J mice were randomly assigned into the control group and the model group. Mice in the model group were given free access to 5% (v/v) alcohol in drinking water, and were intragastrically administered with 28% (v/v) alcohol. The gavage dosage increased gradually over the first two weeks (from 0 to 6 g/kg body weight), and remained at 6 g/kg body weight for the subsequent four weeks. Mice in the control group were provided with normal water and given same amount of saline via gavage. At the end of the experiment, the cognitive function and motor ability of mice were evaluated through behavioral tests. The morphological changes of brain tissue of mice were examined by histopathological staining. Results Compared to the control group, mice in the model group showed cognitive impairments and motor dysfunction in the behavioral tests. The pathological examination of the brain tissue from the model group mice showed morphological damage and cell necrosis in the hippocampus. Conclusions The mouse model of chronic alcoholic brain injury was successfully and effectively established in this study, providing a valuable tool for investigating the underlying mechanisms and potential therapeutic interventions for chronic alcoholic encephalopathy.
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Molecular mechanism and prognosis of patients with HBV infection with DLBCL

Yuanherui, guopengxiang

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In recent years, hepatitis B virus (HBV) infection patients with diffuse large B cell lymphoma (DLBCL) have shown an upward trend, and its etiology is complex and treatment is difficult, so it has received extensive attention from scholars at home and abroad. Based on the review and analysis of the research of domestic and foreign scholars, this paper further discusses the mechanism of the occurrence and development of DLBCL caused by HBV infection and the clinical prognosis of related patients, and finally finds that at the genomic and transcriptome levels, HBV may mainly induce the changes of BCL6, FOXO1, ZFP36L1 and other genes, and activate various regulatory genes through HBV's X protein, thereby inducing clonal proliferation of lymphocytes and eventually forming lymphoma. For the clinical prognosis assessment, the clinical prognosis assessment mainly analyzes and compares the patient's age of onset, sex, organ involvement, international prognostic index (IPI), lactate dehydrogenase (LDH) level, proliferation index (Ki-67), bcl-2, bcl-6, inflammatory index and other factors, aiming to put forward a theoretical basis for the clinical diagnosis and treatment of DLBCL and basic research.
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Study on the mechanism of lncRNA SNHG16 regulating the resistance of hepatoma cells to sorafenib by miR-570

liuyang, Fan Wei, Ding Jie

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Objective: To explore the mechanism of long non-coding RNA SNHG16 (Long non-coding RNA small nucleolar RNA host gene16, lncRNA SNHG16) to anti-liver cancer cell resistance by regulating minimal RNA-570 (miR-570). Methods: The expression of lncRNA SNHG16 and miR-570 of HepG 2 and HepG 2-R cells in human normal liver and hepatoma cells was measured by real-time fluorescence RT-PCR, cell proliferation, apoptosis and invasion were measured by MTT assay, FACS and Transwell test, and cell expression changes of CyclinD1, P21MMP-9 and MMP-2 were determined by Western Blot assay. Results: Compared with normal hepatocytes, lncRNA SNHG16 expression was increased and miR-570 expression was decreased in hepatoma cells (P<0.05). Compared with HepG2-P group, LncRNA SNHG16 and IC50 values were increased in HepG2-R group, and the inhibition rates of miR-570 and HepG2-R cells were decreased at Sorafenib concentrations of 1, 2, 4, 8, 16μmol/L (P<0.05). HepG2-R pcDNA SNHG16 as overexpression group, lncRNA SNHG16 expression was significantly increased (P<0.05), and compared with HepG2-R pcDNA group, In HepG2-R pcDNA SNHG16 group, the number of migrated cells, the expressions of CyclinD1, P21, MMP-9 and MMP-2 were decreased, while the expression of inhibition rate, apoptosis rate and P21 were increased (P<0.05). Compared with HepG2-R anti-miR-NC group, miR-570 level in HepG2-R anti-miR-570 group was decreased (P<0.05), and compared with HepG2-R anti-miR-NC group, HepG2-R anti-miR-570 group decreased the levels of CyclinD1, MMP-9 and MMP-2, and increased the levels of inhibition rate, apoptosis rate and P21 (P<0.05). Dual luciferase reporting experiment showed that compared with miR-NC group, miR-570 reduced the luciferase activity of WT-SNHG16 (P<0.05), but had little effect on the luciferase activity of T-SnHG16 (P>0.05). Overexpression of lncRNA SNHG16 decreased the expression of miR-570 in HepG2-R cells (P<0.05). Compared with HepG2-R pcDNA SNHG16 miR-NC group, In HepG2-R pcDNA SNHG16 miR-570 group, the number of migrated cells, the levels of CyclinD1, MMP-9 and MMP-2 were increased, while the levels of inhibition rate, apoptosis rate and P21 were decreased (P<0.05). Conclusion: By regulating the drug resistance of HepG2-R hepatoma cells, the mechanism is related to the regulation of miR-570 by lncRNA SNHG16, and it can be used as a new target for drug-resistant HCC cell therapy.
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Study on the Mechanism of Hyperuricemia combined with Nonalcoholic Fatty Liver based on PI3K/Akt/NF-kB

gongxiaohong, lihuan

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Abstract: Objective: To study the pathogenesis of hyperuricemia combined with nonalcoholic fatty liver disease (HUA-NAFLD) based on PI3K/Akt/NF-kB signaling pathway. Methods: 64 SD rats were randomly divided into blank group, HUA group, NAFLD group, and HUA-NAFLD group, 16 rats in each group. The samples were collected at the end of the 8th and 12th week, respectively. The serum biochemical indexes of the rats were detected; The pathological changes and lipid deposition in liver tissue were observed by hematoxylin-eosin staining (HE) and Oil Red O staining; the expression levels of PI3K/Akt/NF-kB signaling pathway-related proteins in liver tissue were detected by Western blot. Results: Compared with the other three groups, the liver index of the rats in the HUA-NAFLD group was significantly increased (P<0.05). Compared with the blank group, the levels of UA and LDL in the HUA group were increased, the levels of HDL in the NAFLD group were decreased, the levels of UA, CHOL, TG and LDL in the HUA-NAFLD group were increased, and the levels of HDL were decreased (P＜0.05); Compared with the HUA-NAFLD group, the levels of CHOL, TG and LDL were decreased in the HUA group, and the levels of UA, TG and LDL in the NAFLD group were decreased (P＜0.05). The results of HE and oil red O staining showed that compared with the other three groups, rat liver cells in the HUA-NAFLD group had a large number of fat vacuoles, blurred liver cord structure and more severe lesions. The WB results showed that compared with the blank group, the phosphorylation levels of AKT and p65 in the NAFLD group were significantly increased, and the phosphorylation levels of AKT, PI3K, p65 and IKKβ in the HUA-NAFLD group were significantly increased, and compared with the HUA-NAFLD group, the phosphorylation levels of AKT and p65 in the HUA-NAFLD group decreased significantly(P<0.05). The phosphorylation level of IKKβ decreased significantly in the HUA group, and compared with the HUA group, the phosphorylation level of p65 in the NAFLD group increased significantly (P<0.05). Conclusion: Compared with the single disease group, the HUA-NAFLD group has more abnormal biochemical indexes and more severe liver lesions. The PI3K/Akt/NF-KB signaling pathway may play an important role in the pathogenesis of HUA, NAFLD and HUA-NAFLD.
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Study on Allicin improves human peritoneal mesenchymal cell-mesenchymal transformation induced by high glucose through the JAK2/STAT3 signaling pathway

Gan Linwang, Li Qiancheng, Gao Lichao, Liu Qi, Li Ying, Wang Yujie, Ou Santao

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Objective To investigate the mechanism of allicin in improving human peritoneal mesenchymal cell-mesenchymal transformation induced by high glucose. Methods human peritoneal mesothelial cells (HPMCs) were cultured and divided into two groups. Group 1: ①Control group; ②8.5 mM D-glucose induced group (8.5 mM DG group); ③17 mM D-glucose induced group (17 mM DG group); ④34 mM D-glucose induced group (34 mM DG group); ⑤68 mM D-glucose induced group (68 mM DG group). Except the control group, the other groups were induced with D-glucose of 8.5 mM, 17 mM, 34 mM and 68 mM, respectively, for 48 h. Group 2: ① control group; ②34 mM D-glucose induced group (HG group); ③34 mM D-glucose + low dose allicin induction group (AL-L group); ④34 mM D-glucose + medium dose allicin induction group (AL-M group); ⑤34 mm-glucose + high-dose allicin induction group (AL-H group); ⑥34 mM D-glucose + JAK2 inhibitor induction group (JAK2 group). HG group was induced with 34 mM D-glucose for 48 h, AL-L group, AL-M group and AL-H group were pretreated with 34 mM D-glucose for 6h, and then induced with 10 ng/mL, 20 ng/mL and 40 ng/mL allicin for 48 h, respectively. JAK2 group was pretreated with 1 μmol/L AG490 for 6 h and induced with 34 mM D-glucose for 48 h. The contents of IL-6, TNF-α and IL-1β in HPMCs supernatant were determined by Elisa. CCK-8 was used to detect cell proliferation and morphology. The expressions of JAK2, p-JAK2, STAT3, p-STAT3, N-cadherin, E-cadherin, Vimentin, α-SMA, MCP-1, p65 and p-p65 proteins were detected by Western blot. Results Compared with the control group, the relative survival rate of HPMCs in the high glucose induced group was significantly reduced (P<0.01), and cell morphology was abnormal, the expressions of α-SMA, N-cadherin and Vimentin that promote epithele-mesenchymal transdifferentiation were significantly up-regulated, and the expression of E-cadherin, which inhibits EMT, was significantly down-regulated. JAK2/STAT3 signaling pathway was activated, leading to the occurrence of EMT (P<0.01). Allicin can significantly promote the proliferation of HPMCs induced by high glucose, restore abnormal cell morphology, regulate the level of EMT-related proteins, and improve the epithelial-mesenchymal transdifferentiation of HPMCs. Compared with the high glucose induction group, the pro-inflammatory cytokines IL-1β, IL-6 and TNF-α of HPMCs in allicin treatment group were significantly decreased, and the expressions of pro-inflammatory proteins p-p50 and MCP1 were significantly down-regulated, indicating that allicin could improve the inflammation caused by EMT. Conclution Allicin can improve EMT and inflammation induced by high glucose by inhibiting JAK2/STAT3 signaling pathway to regulate the levels of markers of EMT, inflammatory signaling proteins and inflammatory factors.
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Influence of hyperoside on autophagy in rats with nephrotic syndrome by regulating AMPK/mTOR/ULK1 signaling pathway

kongloujiao, wangxin, liujing, guoxiaoyang, xuemingwei

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Objective To investigate the influences of hypericin (Hyp) on renal autophagy and AMPK/mTOR/ULK1 pathway in nephrotic syndrome (NS) rats. Methods Thirty-two 6-week-old SD rats were grouped into normal group (N group), NS group, Hyp group (60 mg/kg Hyp), Hyp AMPK inhibitor group (Hyp CC group) (60 mg/kg Hyp group) 0.2 mg/kg CC), 8 per group. After administration, an automatic analyzer was applied to detect the levels of 24-h urine total protein (UTP), blood urea nitrogen (BUN), serum creatinine (Scr) and albumin (ALB); HE staining and TEM observation were applied to observe renal pathological morphology and ultrastructure; Western blot was applied to detect the expression of autophagy, podocyte and AMPK/mTOR/ULK1 pathway proteins in kidney; immunofluorescence staining was applied to visualize the localization of autophagosomes and podocytes. Results Compared with the N group, the glomerular volume of the NS group increased, the renal tubules atrophied or partially disappeared, and the basement membrane thickened; UTP, BUN, Scr, basement membrane thickness, foot process width and the ratio of p-AMPK/AMPK were obviously increased (P<0.05), the protein levels of ALB, LC3-II/I, Beclin-1, Atg5, Atg7, NPHS2, the relative fluorescence intensity of NPHS2 and Beclin-1, and the ratios of p-AMPK/AMPK and p-ULK1/ULK1 were obviously decreased (P<0.05). Compared with NS group, Hyp treatment was able to improve glomerular morphology, decrease UTP, BUN, Scr, basement membrane thickness, foot process width and ratio of p-AMPK/AMPK (P<0.05), increase protein levels of ALB, LC3-II/I, Beclin-1, Atg5, Atg7, NPHS2, the relative fluorescence intensity of NPHS2 and Beclin-1 and the ratios of p-AMPK/AMPK and p-ULK1/ULK1 (P<0.05). AMPK inhibitor group CC could attenuate the autophagy-promoting and kidney-protecting effects of Hyp. Conclusion Hyp may enhance the autophagy activity of renal cells and attenuate renal pathology such as podocyte injury in NS rats by activating the AMPK/mTOR/ULK1 pathway.
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Study of core symptom impact on baicalein in an animal model of attention deficit hyperactivity disorder SHR rat

zhang yongting, Zhou Rongyi, Ma Bingxiang, Wu Chenlei, Xie Xinyue, Ding Xueying

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Objective To explore the efficacy and potential mechanism of baicalin in regulating the core clinical symptoms of ADHD through the Morris water maze test and The open field test. Methods Thirty SHR rats were randomly divided into model group, methylphenidate hydrochloride(MPH) group, baicalin group, baicalin + tetrabenazine group and MPH + tetrabenazine group, with 6 rats in each group. Another 6 WKY rats were used as normal control group. The rats in the MPH group (1.5 mg/kg) and the baicalin group(150 mg/kg) were given the corresponding drugs (1 mL/100 g) by gavage, and those in the normal control group and the model group were given an equal volume of normal saline by gavage . In addition to the corresponding drug gavage,the rats in the MPH+tetrabenazine group and the baicalin+tetrabenazine group were given intraperitoneal injection of tetrabenazine(3 mg/kg) according to body weight (0.5 ml/100 g).The course of treatment was 4 weeks for all groups. Open field and Morris water maze experiments were carried out at the specified time, and the experimental results were recorded and analyzed Results In the open field experiment, the total distance and average speed in the MPH group and baicalin group were significantly lower than those in the model group (P < 0.05), and there was no significant difference between the two groups (P > 0.05);In the open field experiment, the total distance and average speed in the baicalin + bubenazine group were significantly lower than those in the model group (P < 0.05), and obviously higher than those in the baicalin group. In the water maze test, the latency of baicalin + bubenazine group was significantly shorter than that in the model group (P < 0.05), and significantly longer than that in the baicalin group (P < 0.05). The percentage of movement distance and stay time in the target quadrant in the baicalin + bubenazine group were obviously higher than those in the model group. It was significantly lower than that in baicalin group (P < 0.05).Conclusion Baicalin can control the core symptoms of hyperactivity, impulse and inattention in SHR rats, and its curative effect may be related to the regulation of dopamine vesicle transport.
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Study on the mechanism of ethyl acetate extract of Liujunzi Decoction on the energy metabolism of EC9706 cells in CAFs conditioned medium

Chen Xing, Lou Xiangyu, Shang Yiwan, Zhou Zhexu, Liu Yang, Liu Yaru, Hu Xiaobo, Chen Yulong

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Objective: To explore the molecular mechanism of ethyl acetate extract of Liujunzi Decoction(EAELD) on energy metabolism of esophageal cancer EC9706 cells in conditioned medium of cancer-associated fibroblasts (CAFs). Methods: Methyl thiazol tetrazolium (MTT) assay was used to detect the effect of EAELD on the proliferation activity of EC9706. The effects of EAELD on lactate and glucose in the supernatant of EC9706 cells in CAFs conditioned medium were detected by colorimetry. seahorse system energy metabolism analysis system was used to detect the effect of EAELD on energy metabolism of EC9706 cells in CAFs conditioned medium. Real-time fluorescent quantitative PCR (q-PCR) and western blotting were used to detect the mRNA and protein expression of energy metabolism-related molecules.. Results: Compared with DMEM, except for the 10μg/mL group,EAELD had a significant inhibitory effect on the proliferation of EC9706 cells (P < 0.05). The inhibitory concentration (IC30) of 25μg/mL and half inhibitory concentration (IC50) of 40μg/mL were selected as the low and high dose groups for subsequent experiments. Among EC9706 cells cultured by CAFM, both low-dose and high-dose EAELD groups could significantly reduce Non-mitochondrial oxygen consumption, Basal respiration value, Maximum respiration value, Oxygen consumption of ATP synthesis, Spare respiration capacity, Basal glycolysis, Compensative glycolysis and glycolysis potential (P <0.01). Decreased the lactate content of EC9706 cells (P <0.01), down-regulated the mRNA expression of GLUT1 (P <0.05, P <0.01), down-regulated the protein expression of p-PKM2, HK2, PKM2 and MCT1 (P <0.01); The high-dose EAELD group could down-regulate the Mitochondrial oxygen consumption and basal use The glycolytic ratio of EC9706 cells (P <0.05), reduce glucose uptake of EC9706 cells (P <0.05), down-regulate the protein expression of p-PKM2 and GLUT1 (P <0.01, P <0.05); The low dose group of EAELD could down-regulate the mRNA expression of MCT1 (P <0.05). Conclusions:EAELD can interfere with the energy metabolism of EC9706 cells in CAFs conditioned medium, and its mechanism may be related to the regulation of HK2, PKM2, GLUT1, MCT1 and MCT4 mRNA and protein expression.
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Application characteristics of animal model of osteosarcoma based on data mining

yushuaike, luomaoli, wanglianrui, zhoutianbao, baili, miaomingsan

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Objective To summarize the key points of animal modeling of osteosarcoma, and to provide reference and suggestions for improving the modeling methods and evaluation indexes.Methods The database was established by searching the relevant literature on the animal model of osteosarcoma in CNKI, Wanfang database and PubMed. The species of experimental animals, gender, modeling methods, types of cancer cell lines and detection indicators were summarized, and the database was established for statistical analysis. Results A total of 284 literatures were included. Statistical analysis found that BALB / c-nu / nu nude mice were preferred in osteosarcoma model animals(227 cases，75.17%), followed by SD rats (20 cases, 6.62%). Subcutaneous cell fluid transplantation in the back (66 cases, 21.85%), subcutaneous cell fluid transplantation in the axils (55 cases, 18.21%) or in situ cell fluid transplantation (51 cases, 16.89%) were used as modeling methods. Human MG-63 cells (100 cases, 33.11%) and mouse UMR-106 cells (39 cases, 12.91%) were selected as the cancer cell lines.The most detected indexes were tumor tissue apparent index (238 cases, 83.80%), tumor tissue HE staining (129 cases, 45.42%), Animal apparent indicator (94 cases, 33.10%)，tumor tissue immunohistochemistry (89 cases, 31.34%), etc. Conclusions At present, osteosarcoma BALB / c-nu / nu nude mice aged 4 to 6 weeks are used as experimental animals, and human MG-63 cell heterotopic transplantation (back and axillary transplantation) is used to establish the animal model, and the detection indexes of osteosarcoma are comprehensively evaluated by animal apparent index, tumor apparent index and tumor histopathology. It is suggested to select serum biochemical index, apparent index of tumor tissue as well, HE staining of tumor tissue and immunohistochemistry of tumor tissue to evaluate the model. However, there is still a lack of animal model preparation and evaluation criteria with high clinical consistency. In this paper, the advantages and disadvantages are summarized through literature mining and data analysis, in order to provide reference for the establishment of a good OS model and better application to OS mechanism research and new drug development.
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Effects of moderate intensity and high intensity intermittent exercise on myocardial mitochondria autophagy in mice with nonalcoholic fatty liver disease

he miao, li jia hang, liu xin, yang wei, wu liang wen, fan jing jing

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Objective To investigate the effects of moderate aerobic exercise and high intensity intermittent exercise on myocardial mitochondria autophagy in mice with non-alcoholic fatty liver disease and its possible mechanism. Methods Forty 3-week-old male C57BL/6J mice were randomly divided into normal feeding group (Chow group, n=10) and high fat feeding group (HFD group, n=30). At week 18, those whose body weight in HFD group exceeded 20%~30% (including 20%) of the ordinary diet group were judged as obese mice (n=26). Two mice were randomly selected for liver oil red O staining to confirm the successful establishment of NAFLD mouse model. Sixteen NAFLD mice were randomly selected and divided into moderate intensity aerobic exercise group (MICT group) and high intensity intermittent aerobic exercise group (HIIT group), with 8 mice in each group. The two groups were given exercise training for 8 weeks, respectively, and the samples were weighed after intervention. Masson staining was used to observe myocardial fibrosis. The ultrastructure of myocardial cells was observed by transmission electron microscopy. Mitochondrial autophagy and mitochondrial biogenesis were detected by Western Blot. Results ⑴ Compared with Chow group, body weight and heart index in HFD group were significantly increased and decreased. Compared with HFD group, the body weight of MICT and HIIT group increased significantly, and the heart index of MICT group increased. (2) Masson results showed that compared with Chow group, the content of collagen fibers in myocardium in HFD group was significantly increased, and the myocardial fibers were disorganized and broken under electron microscope. The morphology of myocardium was disorganized, mitochondria were swollen, crists were broken and blurred, and lipid droplets were included. Compared with HFD group, the myocardial collagen fiber content in MICT and HIIT groups was significantly reduced, the myocardial fiber arrangement was slightly recovered under transmission electron microscopy, the Z-line was clearly visible, the degree of mitochondrial degeneration was slightly improved, and the lipid droplets were also slightly reduced. Among them, the improvement effect of MICT group on the cardiac tissue structure was better than that of HIIT group. (3) Western Blot results showed that compared with Chow group, the expression levels of PINK1 and Beclin1 in myocardial tissue of HFD group had no significant changes, while the expressions of Parkin, LAMP1 and PGC-1α were significantly decreased (p<0.01). p62 protein expression and LC3-II/LC3-I ratio were significantly increased (p<0.05, p<0.01); Compared with HFD group, the expression levels of PINK1 and Beclin1 in MICT and HIIT groups were not significantly changed, while the expression of PGC-1α was up-regulated, and the expressions of Parkin and LAMP1 in MICT group were significantly increased (p<0.05). p62 protein expression and LC3-II/LC3-I ratio were significantly decreased (p<0.05, p<0.01), Parkin and LAMP1 expression levels were up-regulated, LC3-II/LC3-I ratio and p62 protein expression were significantly decreased in HIIT group (p<0.05, p<0.01). Conclusion Different forms of aerobic exercise can effectively ameliorate myocardial structural and functional injury in NAFLD mice, which may be through stimulating the autophagy flux of mitochondria in cardiomyocytes, activating autophagy and restoring the normal autophagy function of cells, so as to ameliorate myocardial cell damage, and moderate continuous aerobic exercise has better improvement effect.
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Exploring the Management Innovation Mechanism of Emergency Science and Technology Research Projects in the Medical Field

CHEN Yujun, SU Meiyangyi, WANG Qingxuan, GAO Ran

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Objective The emergency technology research project highlights the two key aspects of "emergency" and "research", which are how to effectively achieve the goal results.Organizations that undertake such projects need to develop reasonable project management mechanisms to ensure the successful implementation of emergency technology research projects.This article aims to investigate the current problems in the management of emergency technology research projects in the medical field through research, analyze possible improvement measures, and improve the efficiency and quality of scientific research management.Methods This article combines the author's practical experience, investigates the current status of scientific research management in relevant units, and conducts questionnaire surveys on the management aspects that are most concerned by scientific management and researchers.Based on the problems reflected in the survey, experts are organized to discuss and demonstrate.Results Through the research, it is found that: 1. At present, there are few management norms for emergency technology research projects;2. The most concerned issue for scientific researchers is administrative approval and project funding;3. The most concerned issue for scientific management personnel is how to meet the management requirements of higher-level units and the needs of scientific researchers under the premise of legal compliance.Conclusion Emergency technology research projects have their own unique characteristics compared to conventional technology projects. Management optimization can be carried out in terms of project approval, fund use, resource allocation, and safety. This study provides innovative solutions for the management of emergency technology research projects, and provides useful experience and reference for various scientific research units in managing such projects.
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Effects of compound active tea of Lithocarpus litseifolius on uric acid and renal function in mice with hyperuricemia nephropathy

陈, zengyanan, DUXIAOLANG, MUZEJING, liaochengdong, zhangchanghua, caolan

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Abstract：Objective To explore the effect of compound active tea of Lithocarpus litseifolius on uric acid and kidney function on mice with hyperuricemia nephropathy , and to provide experimental basis for the development of hyperuricemia nephropathy drugs and functional food. Methods The mouse model of hyperuricemia nephropathy was established by potassium oxyoxide with adenine. Mice were randomly divided into normal group, model group, benbromarone positive drug group (10 mg?kg-1?d-1), and Compound active tea of Lithocarpus litseifolius high,middle, low-dose groups (10g?kg-1?d-1,3.33g?kg-1?d-1,1.11g?kg-1?d-1).1h after the last dose, urine protein (UP) was measured by CBB method,urea nitrogen (UUN) was measured by the urease method;Blood was collected for uric acid (UA) by enzyme ratio method and urea nitrogen (BUN) by urease method;the serum content of interleukin cells 6 (IL-6) and tumor necrosis factor(TNF-α) was measured byeuzymelinked immunosorbent assay;uate transporter 1 (URAT1) and glucose transporter 9 (GLUT9) in mouse kidneys were measured by quantitative fluorescence analysis.Kidney tissues were harvested and histopathological changes were observed by HE staining.Results Compared with the normal group,the UP, UUN, UA, BUN, IL,URAT1 and ULUT9 of model group mice were significant increased (P<0.01),TNF-α was increased (P<0.05),the renal tissue structure was normal.Compared with the model group,the UP,UUN,UA,BUN of benbromarone positive drug group were significant decreased(P<0.01),IL-6 and TNF-α were decreased(P<0.05),URAT1 was increased(P<0.05),little glomerular atrophy and deformation in the kidney,kidney tubular dilatation was occasionally seen,and no inflammatory cell infiltration.Compared with the model group,the UP,UUN,UA,BUN,IL-6 and URAT1 of high-dose group of compound active tea of Lithocarpus litseifolius were significant decreased(P<0.01),TNF-α and GLUT9 levels were decreased(P <0.05);the UP, UA, UUN content , the levels of IL-6, URAT 1and GLUT9 of middle-dose group of compound active tea of Lithocarpus litseifolius were significant decreased(P<0.01),BUN together with reduced levels of TNF-α(P <0.05);the UP,UUN,UA,IL-6 and URAT1 of low-dose group of compound active tea of Lithocarpus litseifoliuswere significant decreased(P<0.01),BUN content and reduction of TNF-α and GLUT9 levels (P<0.05),the kidney condition of the mice in compound active tea of Lithocarpus litseifolius group was improved.Conclusion: the compound active tea of Lithocarpus litseifolius can reduce uric acid in mice with hyperuricemia nephropathy, and it has a certain protective effect on the kidney,the mechanism may be related to the inhibition of uric acid reabsorption, and the specific mechanism should be further investigated.
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HDAC6 inhibitors improve diabetic nephropathy by protecting glomerular endothelial cell mitochondria

ChenXiaoli

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objective: To investigate the protective effect and mechanism of histone deacetylase 6 (HDAC6) specific small molecule inhibitor Tubastatin A on renal injury in diabetic nephropathy (DN) mice. Methods: C57BL/6 mice were randomly divided into 3 groups: control group, DN group and Tubastatin A group. Mice in the DN group and Tubastatin A group were intraperitoneally injected with燬TZ?80爉g/kg) daily for 3 days after the removal of one kidney. Tubastatin A group received Tubastatin A treatment every 3 days for 8 weeks. RNA sequencing analysis of differentially expressed genes in kidney tissue of DN group and Tubastatin A group. Mitochondrial damage was assessed by transmission electron microscopy, and ROS levels in kidney tissue were estimated by DHE staining. Mouse glomerular endothelial cells (mGEC) were exposed to high glucose medium (HG) or 40 mM mannitol (control) with or without Tubastatin A treatment. Western blot analysis was used to analyze the expression of HDAC6, kidney injury markers KIM1 and EMT markers, and flow cytometry was used to detect mitochondrial ROS and apoptosis in cells. Results: HDAC6 expression was up-regulated in DN mouse kidney tissue and mGEC cells exposed to HG, consistent with increased levels of KIM1. Histological analysis showed significant morphological changes in DN mice, including glomerular hypertrophy, mesangial matrix accumulation, glomerular basement membrane thickening, tubular basement membrane thickening and the presence of glomerular, intertubular fibrosis; Tubastatin A treatment alleviated these changes. Compared with control DMSO, Tubastatin A significantly decreased the expression of KIM1, HDAC6, α-SMA, N-cadherin, vimentin (P<0.05) and up-regulated the expression of E-cadherin (P<0.05) in mGEC cells under HG treatment. RNA-sequencing revealed the enrichment of genes related to ECM-receptor interaction and tricarboxylic acid (TCA) cycle in the kidney tissue of Tubastatin A mice compared with DN mice. Transmission electron microscopy showed that the proportion of damaged mitochondria in glomerular endothelial cells in Tubastatin A group was significantly lower than that in DN group (P<0.01). DHE staining showed that the level of ROS in the kidney tissue of Tubastatin A group was lower than that of DN group (P<0.01). In mGEC cells, Tubastatin A treatment down-regulated HG-induced mitochondrial ROS levels in mGEC cells (P<0.01), and reduced apoptosis (P<0.05). Conclusion: Tubastatin A ameliorates HG-induced glomerular endothelial cell injury and DN progression, and its mechanism is related to the protection of mitochondrial homeostasis and inhibition of EMT.
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Effects of human amniotic epithelial cells transplantation on the improvement of endometrium and MMP-8, VEGF in rat model of uterine scar

王静

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Objective: To investigate the effect of human amniotic epithelial cells (hAECs) transplantation on endometrium improvement and matrix metalloproteinase-8 (MMP-8) and vascular endothelial growth factor (VEGF) in a rat model of uterine scar. Methods: The uterine scar model of rats was established and randomly divided into model group and transplantation group, with 18 rats in each group. The other 18 rats were selected as sham operation group. The rats in the transplantation group were injected with hAECs in the scar of the uterus, and the rats in the model group and the sham operation group were only given the same amount of PBS. After 4 weeks, the uterine tissues of 8 rats in each group were collected and HE staining was used to observe the histomorphological changes, and the endometrial thickness and the number of glands were measured. Masson staining was used to observe endometrial fibrosis. Endometrial growth and receptivity were evaluated by immunohistochemical staining for cytokeratin and integrin β3, respectively. The mRNA expression levels of MMP-8 and VEGFA in endometrial tissues were detected by RT-qPCR. Western blotting was used to detect the protein expression levels of MMP-8 and VEGFA. After 8 weeks, the remaining 10 rats in each group were selected for gestational ability determination. Results: Compared with the sham-operation group, the endometrial thickness, the number of glands, the IOD value of keratin and integrin β3, the mRNA and protein relative expression levels of MMP-8 and VEGFA, the pregnancy rate and the number of uterine embryos in the model group and the transplantation group were significantly decreased (P<0.05). Compared with the model group, the endometrial thickness, the number of glands, the IOD value of keratin and integrin β3, the mRNA and protein relative expression levels of MMP-8 and VEGFA, the pregnancy rate and the number of uterine embryos were significantly increased in the transplantation group (P<0.05). In addition, hAECs transplantation could improve the pathological morphology of endometrial tissue in rats with uterine scar. Reduce the degree of endometrial fibrosis. Conclusion: hAECs transplantation could improve endometrial injury, reduce scar formation, improve endometrial receptivity, and enhance pregnancy function in model rats, which may be related to the promotion of MMP-8 and VEGFA expression.
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Effect of inhibition of the mitochondrial inner membrane protein OMA1 on apoptosis in a Rot-induced Parkinson's disease cell model

shijin, Lihaining, Luyue, Xuting

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Objective To investigate the effect of inhibition the mitochondrial inner membrane protein OMA1 on rotenone-induced apoptosis in Parkinson's disease (PD) cell model. Methods SH-SY5Y cells were cultured in vitro, treated with Rot (final concentrations of 0.05, 0.1, 0.2, 0.3, 0.4 μmol/L) for 24 h, and the best Rot (0.2 μmol/L) was selected for subsequent experiments. The experiment was divided into control group (cells without special treatment), PD model group (0.2 μmol/L Rot treated cells for 24 h), Negative control group (negative control sequence of OMA1 siRNA transfected on the basis of normal control group), OMA1 siRNA group (0.2 μmol/L Rot treated cells for 24 h and transfected with OMA1 siRNA). CCK-8 was used to detect cell survival rate, inverted phase contrast microscope was used to observe cell morphology in each group, Western blot was used to detect changes in the expression of OMA1 and apoptosis-related proteins Caspase-3, Bax, and Bcl-2, and TUNEL apoptosis kit was used to detect cell apoptosis. Results Compared with the control group, the survival rate of SH-SY5Y cells decreased in a concentration-dependent manner with increasing Rot concentration (P<0.05). Compared with the control group, the expression of OMA1 and apoptotic protein Caspase-3 expression were increased and Bax/Bcl-2 values were increased in the PD model group (P<0.01). Compared with the PD model group, the cells in the OMA1 siRNA group, the OMA1 siRNA group gradually restored morphological changes, decreased apoptotic protein Caspase-3 expression and Bax/Bcl-2 values, and TUNEL apoptosis staining suggested reduced apoptosis (P<0.01). Conclusions Inhibition of the mitochondrial inner membrane protein OMA1 ameliorates apoptosis induced by the Rot-induced PD cell model, which in turn may have a protective effect on neurons.
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The effect of CeO2NPs on organ structures and redox indicators in male mice

yin jun

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Objective To investigate the effects of CeO2NPs sub-acute exposure on body weight, organ structures and redox indicators in male mice. Methods 35 male ICR mice were randomly divided into five groups with seven mice in each group. Normal control group and CeO2NPs (100, 500, 1000, 5000 ug/kg) test groups were set up. Mice were injected CeO2NPs intraperitoneally every other day for 28 days. Results Compared with the control group, there was no significant difference in weight gain (P>0.05) , but there was significant difference in liver coefficient, epididymal coefficient and sperm survival rate (P<0.01). In the 5000 ug/kg group, CeO2NPs were deposited in the liver and spleen, and granuloma was found. The activities of SOD and GSH-Px in serum of 100 ug/kg group were increased, while the content of MDA was decreased, which showed the antioxidant effect of CeO2NPs. With the increase of dose, the oxidative stress induced by CeO2NPs was enhanced. Conclusion The low dose of CeO2NPs is safe and has antioxidant effect. With the increase of dose, the toxicity of CeO2NPs to the body also increases gradually.
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Research progress on gut microbiota and obesity-related metabolic diseases

Su Hei Yan Pa Er Ha Ti, ZHANG Jiaojiao, MA Zhuang, WANG Junren, LI Yanhong

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Obesity centered metabolic diseases such as diabetes, hypertension, and cancer are increasing at an alarming rate worldwide and have become global public health concerns. The treatment of obesity and related metabolic diseases has gradually become a research hotspot. Currently, an increasing number of studies have proved that gut microbiota can regulate energy balance and glycolipid metabolism, and regulate the occurrence and development of obesity and related metabolic diseases. It is very likely that the gut microbiota is a potential new target for the treatment and prevention of metabolic diseases. In this paper, we summarize the progress of gut microbiota in the development and progression of obesity associated metabolic diseases and analyze the role of gut microbiota in metabolic diseases.
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Research progress of exosomal microRNA in early screening and treatment of Alzheimer's disease

zhangjunfeng

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Exosomes, as small molecule extracellular vesicles secreted by a variety of cells, play an important role in the pathological process of Alzheimer's disease by transporting a variety of bioactive substances such as microRNA. Studies have shown that the expression of exosomal microRNA changes in the early stages of AD patients, and exogenous injection of mesenchymal stem cell-derived exosomal microRNA can improve the learning and memory ability of AD animal models. This paper reviews the research progross of exosomes in early screening and treatment of Alzheimer's disease.
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Research progress of disease-syndrome combination models of chronic obstructive pulmonary disease

badeting, HAO Binbin, LI Juan

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Chronic obstructive pulmonary disease (COPD) is a common respiratory disease with high morbidity and mortality, which has become an important health problem in today's society. Traditionray Chinese Medicine has accumulated rich historical experience in the treatment of COPD and has unique clinical advantages. In order to further explore the therapeutic effect of traditional Chinese medicine on this disease, the preparation of COPD animal model combining disease and syndrome is the key premise of studying the occurrence and development of the disease. The combined models of disease and syndrome summarized in this paper include five types: the animal model of lung qi deficiency, the animal model of lung and spleen deficiency, the animal model of phlegm-heat stagnation of lung, the animal model of phlegm-stasis obstructing lung, and the animal model of cold drink. Now the common disease and syndrome in recent years combined with the method of class modeling are simply described and combed, in order to provide new ideas for researchers, and promote the research process of traditional Chinese medicine treatment of this disease.
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Research Progresses on the Effects of the Plateau on Mitochondrial Function and Energy Metabolism

LIBOSHEN, ZHANGYUXUAN, FANRONGHUI, LIMAOXING

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The plateau is a unique environment with low pressure, low oxygen and high cold. The plateau environment will reduce the metabolism of energy substances and mitochondrial work, thus affecting the plateau operation. In recent years, mitochondrial damage has attracted wide attention. As the energy factory of cells, mitochondria are closely linked to the movement of the body. We focused our attention on mitochondrial damage at high altitude, and summarized the effects of high altitude on the metabolism of basic energy substances and the changes of key enzyme activities and mitochondrial structure and function in mitochondrial biochemical energy supply response. It was found that protein, carbohydrate and lipid metabolism was negatively affected at high altitude, resulting in fatigue, hyperlipidemia and body repair. The activities of enzymes related to pyruvate metabolism, tricarboxylic acid cycle, β-oxidation and oxidative phosphorylation are inhibited, and the morphology and number of mitochondria are changed, which will lead to impaired mitochondrial function and affect exercise energy supply. In the future, the exploration of the mechanism of plateau cell injury will vigorously promote the research of plateau injury prevention and treatment drugs.
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A review of animal models of vascular dementia

songyuanyu, chenyinghua

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Abstract: Vascular Dementia (VD) is caused by cerebrovascular diseases, either hemorrhage or ischemic damage in the brain, with ischemia being the most common. In recent years, much more efforts have been made to study the etiology, pathogenesis and prevention of VD. The establishment of appropriate animal models for studying the mechanism of VD and exploring efficacy of VD treatment has become one of key issues in the research field. On the basis of the conventional methods such as the bilateral occlusion of the common carotid arteries (2VO) and the four-vessel occlusion, the researchers had modified these methods to improve the stability with better reflection of the clinical manifestations of VD. This paper mainly summaries these modified methods, and discuss possible cellular and molecular mechanisms and their advantages and disadvantages.
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Keratin 17 knockout aggravates wound healing in diabetic mice

Bao Dan, Guo Rui, Hou Daorong

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Objective To explore the effects of keratin 17 (Krt17) knockout on wound healing in diabetic mice. Methods To establish the diabetic models, 60% high-fat diet was fed and streptozotocin was administered intraperitoneally at 40mg/kg once per day for 5 consecutive days in wild-type (WT) and Krt17 knockout (Krt17-/-) mice at six weeks of age. The mice were anesthetized with isoflurane, the back was shaved, and a 6 mm circular skin lesion was made in vivo at one week after successful modeling. Western blotting and immunofluorescence staining were used to detect the expression and localization of KRT17 and histopathological examination was analyzed in wound healing on the 8th day. Photos were taken at 0, 2, 4, 6 and 8 days after wound manufacturing, and wound healing rate was calculated. Results KRT17 was mainly expressed in mouse hair follicles in physiological conditions. When the skin was injured, the expression of KRT17 in keratinocytes in the proximal wound was significantly increased. However, the expression of KRT17 in wounds of diabetic mice was significantly down-regulated compared with that of control mice. The wound healing rate of Krt17-/- mice was significantly reduced and the local inflammatory reaction was more persistent compared with WT mice. Conclusions Krt17 knockout aggravates wound healing in diabetic mice. Krt17 may be an important modifier gene of diabetic wound healing.
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Effects of baicalin on proliferation and apoptosis of laryngeal cancer cells via miR-125b-5p/IRF4 axis

WANGJIAN, SUNYONGDONG, ZHOUXINGWEI, LIULEI, TONGXINGKE, CHENLONG, HEXIAN

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Objective: To explore the mechanism of baicalein inhibiting the proliferation and migration of laryngeal cancer cells. Methods: Hep-2 cells were used as the research object. The cell proliferation activity of each group was detected by MTT method, cell migration was detected by scratch assay, cell apoptosis was detected by flow cytometry, western blot was used to detect the expression levels of Beclin-1, LC3II/I, p62 and HDAC1 in laryngeal cancer cells in each group, RT-PCR detection of the expression levels of miR-449a in each group of cells. The targeted binding sites of miR-449a and HDAC1 were analyzed by bioinformatics software and identified by dual luciferase reporter gene experiments. The number of autophagosomes was observed by projection microscopy. Results: Baicalein significantly inhibited the proliferation and migration of laryngeal cancer cells, and significantly induced apoptosis. Baicalein increased the protein expression levels of intracellular autophagy-related genes Beclin1 and LC3II, but decreased the protein expression levels of p62 and LC3I. Baicalein significantly increased the expression level of miR-449a in laryngeal cancer cells and decreased the protein expression of HDAC1. There is a binding effect between HDAC1 and miR-449a. Baicalein combined with miR-449a mimic to treat laryngeal cancer cells can more significantly inhibit cell proliferation and HDAC1 protein expression, as well as more effectively up-regulate the relative expression of miR-449a and induce autophagy. Conclusion: Baicalein can mediate autophagy and inhibit the proliferation and migration of laryngeal cancer cells via the miR449a/HDAC1 axis.
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Effects of low-dose BPA and DEHP on the expression of AKR1C3 in prostate of adult rats

Huangdongyan, Wushuangshuang, Shaocongcong, Suxin, Yangrongfu, Wangkaiyue, Zhouping, Wujianhui

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Objective To investigate the effects of of low dose of bisphenol A (BPA) and di (2-ethyl) hexyl phthalate (DEHP) on Aldo-keto reductase 1C3 (AKR1C3) in adult SD rats. Method 56 adult male SD rats were randomly divided into 7groups (8 rats in each group) and they were given BPA (10.0µg/kg,30.0µg/kg,90µg/kg, i.g.), DEHP (30.0µg/kg ,90.0µg/kg ,270 µg/kg, i.g.) and vehicle respectively once a day for 4 weeks. The animals were sacrificed on the day subsequent to last treatment and the blood was collected, the prostate tissues were dissected and categorized into different lobes. The levels of AKR1C3 in serum and prostate were detected by enzyme-linked immunosorbent assay (ELISA), and the expression of AKR1C3 in each lobe of prostate was analyzed by immunohistochemistry. Result After the administration of BPA, the expression of AKR1C3 in 90µg/kg and 270µg/kg group increased, and there was significant difference in the high-dose group (P<0.05); The level and protein expression of AKR1C3 in dorsal prostate increased, and there was significant difference in 10µg/kg group (P<0.01, P<0.001). After administration of DEHP, the level of serum AKR1C3 in 270µg/kg group was significantly higher than that in the control group (P<0.001), the level of AKR1C3 in the ventral prostate was significantly higher than that in the control group (P<0.05, P<0.01), and the expression of AKR1C3 protein increased, there was significant difference in 270µg/kg group (P<0.05); The level of AKR1C3 in 90µg/kg and 270µg/kg dose group of dorsal prostate was higher than that in the control group, and there was significant difference in 30µg/kg group (P<0.05). The expression of AKR1C3 protein in each group increased, and there was significant difference in 30µg/kg and 90µg/kg dose group (P<0.001, P<0.05). Conclusion Low-dose BPA and DEHP can promote the expression of AKR1C3 in the prostate of adult SD rats, but the sensitivity of ventral and dorsal lobes of prostate to BPA and DEHP is different.
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Bone marrow mesenchymal stem cells isolated from rats by bone marrow and slice adherent culture in vitro and PKH26 labeling

Chen Shuang, Yan Zhenyu

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Objective To establish an efficient method for isolation and culture of rat bone marrow mesenchymal stem cells (BMSCs), and apply PKH26 to label them in vitro to explore the effect of PKH26 labeling on the biological characteristics of BMSCs, as well as the in vitro tracing. Methods The bone of both hind limbs of 5d suckling rats were separated, the surrounding muscle and fascia were removed, and cut into small pieces for culture. BMSCs were purified by fluid exchange and passage, and the third generation cell surface antigen was determined by flow cytometry. Under the same culture conditions, the third generation BMSCs were labeled with PKH26. Cell morphology and proliferation status were observed under fluorescence microscope in the labeled group and the unlabeled group, and the adipogenic induction characteristics and identification of the labeled group and the unlabeled group were compared. Results The bone marrow slice method was used to separate the hind limb bones of suckling mice. The BMSCs were slender spindle shaped and uniform in shape. A large number of BMSCs could be rapidly obtained in a short time; The results of flow cytometry showed that the expression of CD29 was (91.18 ± 1.29)%, the expression of CD90 was (91.18 ± 1.29)%, and the expression of CD45 was (1.74 ± 0.36)%; PHK26 labeling had no significant effect on the morphology and proliferation of BMSCs cells (P>0.05), and had no effect on the induction of osteogenesis and adipogenesis. Conclusions A large number of high-purity BMSCs can be rapidly cultured by the method of 5-day rat bone marrow slices, which can be used as seed cells for bone tissue engineering; PKH26 can label rat BMSCs in vitro.
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Regulation of ADAM10 gene osteogenic differentiation of bone marrow mesenchymal stem cells and tibial fracture union through Notch1 pathway

TangXiaoxu, Liu wanting, Douyinxia, Li Fuqin, Wang Nan

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Objective To study the regulation of a disintegrin and metalloproteinase 10 (ADAM10) gene on osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and tibial fracture union. Methods BMSCs of SD rats were cultured, BMSCs stably transfected with negative control (NC) shRNA or ADAM10 shRNA pGFP-V-RS vector were established, the osteogenesis was induced for 14 days. During the induction process, DMSO or 10 μmol/L Notch1 agonist valproic acid (VPA) were added. absorbance at 405nm of alizarin red staining, ALP activity and the expression levels of ADAM10, OCN, Runx2, CoL-I, NICD and Hes1 were detected. The tibial fracture model of SD rats was established and NC shRNA or ADAM10 shRNA pCMV5.0 vector was injected locally. The fracture healing and gene expression were observed for 4 weeks later. Results The expression level of ADAM10 in BMSCs in sh-ADAM10 group was lower than that in sh-NC group. After osteogenesis induction, the absorbance value of alizarin red staining at 405nm, ALP activity and the expression levels of OCN, Runx2, CoL-I, NICD and Hes1 of sh-ADAM10 group were higher than those in sh-NC group (P<0.05). the absorbance value of alizarin red staining at 405nm, ALP activity and the expression levels of OCN, Runx2, CoL-I of sh-ADAM10 VPA group after osteogenesis induction were lower than those in sh-ADAM DMSO group (P < 0.05). The fracture healing of tibial fracture rats in sh-ADAM10 group was better than that in sh-NC group, and the expression levels of OCN, Runx2, CoL-I, NICD and Hes1 were higher than those in sh-NC group (P<0.05). Conclusion Knockdown of ADAM10 can promote the osteogenic differentiation of BMSCs and the healing of tibial fractures by inhibiting Notch1 pathway.
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The improvement effect and mechanism of modified Chaihu Guizhi Decoction on osteoporosis rats by regulating Wnt/β-catenin signaling pathway

Guo Zhonghua, Cao Yuju

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Objective: To investigate the improvement effect of modified Chaihu Guizhi Decoction (CGD) on osteoporosis rats by regulating the Wnt/β-catenin signaling pathway. Methods: SD rats were separated into CK group, Model group, low-dose CGD group (CGD-L group, 5 g/kg), high-dose CGD group (CGD-H group, 20 g/kg), and estradiol valerate group (EV group, 9 mg/kg), DKK-1 (Wnt/β-catenin pathway inhibitor) group (100 mg/kg), and CGD-H DKK-1 group (20 g/kg 100 mg/kg), 12 per group. Except for the CK group, the rats in other groups were given 70 mg/kg retinoic acid to build the OP rat model, and the rats in the CK group were given the same amount of normal saline. From the 4th week of modeling, the corresponding drug intervention was given for 4 weeks. ELISA was applied to detect the levels of collagen type I C-terminal peptide (CTX-Ⅰ) and osteocalcin (BGP) in serum of rats; the changes of bone volume fraction, bone trabecular thickness, bone mineral density and bone trabecular number were observed; HE staining was applied to detect the pathological changes of rat femur; Alkaline phosphatase (ALP) calcium-cobalt staining was applied to detect osteoblast activity in rat femur; the activity of osteoclasts in rat femur tissue was detected by tartrate-resistant acid phosphatase (TRAP) staining; Western blot was applied to detect Wnt and β-catenin proteins in femoral tissue of rats in each group. Results: Compared with the CK group, the femoral tissue of the Model group had severe pathological damage, CTX-I level and osteoclast activity increased, BGP level, bone volume fraction, bone trabecular thickness, bone mineral density, bone trabecular number, osteoblast activity, Wnt, β-catenin protein expression decreased (P<0.05); compared with the Model group, the pathological damage of the femur in the CGD-L group, the CGD-H group and the EV group was alleviated, CTX-I level and osteoclast activity decreased, BGP level, bone volume fraction, trabecular thickness, bone mineral density, bone trabecular number, osteoblast activity, Wnt, β-catenin protein expression increased, the trends of the corresponding indicators in the DKK-1 group were opposite to the above (P<0.05); compared with the CGD-H group, the femoral tissue of the CGD-H DKK-1 group was severely damaged, CTX-I level and osteoclast activity increased, BGP level, bone volume fraction, bone trabecular thickness, bone mineral density, bone trabecular number, osteoblast activity, Wnt, β-catenin protein expression decreased (P<0.05). Conclusion: CGD may improve OP of rats by activating the Wnt/β-Catenin pathway.
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Acupoint catgut embedding affects the level of inflammation in rheumatoid arthritis through PD-1/OX40 signaling pathway

Chen Li-chuan, Duan bo, Yu Zhao, Ma Zhi-yi, Meng Qian-wen

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Objective: This experiment studied the effect and mechanism of acupoint catgut embedding on rheumatoid arthritis by regulating PD-1 / OX40 signal pathway. Methods: 25 female SD rats were induced with complete Freund's adjuvant to establish rheumatoid arthritis model rats, and then treated with acupoint catgut embedding and drug therapy. The rats were divided into 5 groups: control group, model group, leflunomide group, acupoint catgut embedding group and acupoint catgut embedding leflunomide group. The degree of inflammation was judged by evaluating the arthritis index; The contents of serum IL-6 and IL-8 were detected by ELISA; He staining was used to observe synovitis cell infiltration, smooth abdominal tissue, fibrous tissue, macrophage proliferation and angiogenesis; The contents of PD-1 / OX40 and CD4 cd28-pd-1lowox40 T cell subsets were detected by flow cytometry. Results: except the control group, there were erythema and moderate swelling from ankle to metatarsal or metacarpal joint in each group. After 14 days, there was no significant change in the score of the model group, but the inflammatory factor scores of leflunomide group, acupoint catgut embedding group and acupoint catgut embedding leflunomide group began to decline, and the acupoint catgut embedding leflunomide group decreased the fastest. The contents of IL-6 and IL-8 in serum of model group increased significantly (P < 0.01), and the contents of IL-6 and IL-8 in serum of rats in flutamide group, acupoint catgut embedding group and acupoint catgut embedding leflunomide group decreased significantly (P < 0.01). The synovial tissue of the model group was damaged, with a large number of inflammatory cell infiltration, vascular dilatation and fibroblast proliferation. After leflunomide and acupoint catgut embedding treatment, the inflammatory cell infiltration in the synovial tissue of the model group was significantly reduced and the vascular proliferation was inhibited, and the effect was the most obvious when Leflunomide and acupoint catgut embedding worked together. In the model group, the content of pd-1lowox40 decreased significantly (P < 0.01), the content of CD4 cd28-pd-1lowox40 T cells increased significantly (P < 0.01), and the content of pd-1lowox40 in acupoint catgut embedding group and leflunomide acupoint catgut embedding group increased significantly (P < 0.01) The content of CD4 cd28-pd-1lowox40 T cells in acupoint catgut embedding group and acupoint catgut embedding leflunomide group decreased significantly (P < 0.01). Conclusion: acupoint catgut embedding can improve the symptoms of rheumatoid arthritis, and has the effect of combined treatment with leflunomide. Its mechanism may be related to PD-1 / OX40 signal pathway.
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Left to right shunt slows cardiac remodeling in rats with pulmonary hypertension

jishuang

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【Abstract】Objective: The prognosis of patients with left-to-right shunt congenital heart disease associated pulmonary hypertension is significantly better than that of idiopathic pulmonary hypertension, but the specific mechanism is unclear. The purpose of this project is to make a rat model of idiopathic pulmonary hypertension and congenital heart disease with pulmonary hypertension, and compare the similarities and differences between the two models in pulmonary vascular remodeling and cardiac remodeling. Methods: Male SD rats were divided into three groups: control group (n=8), monocrotaline (MCT) group (50mg/kg) to simulate idiopathic pulmonary hypertension (n=8); Cervical arteriovenous shunt surgery monocrotaline (MCT) group (50mg/kg) simulated left to right shunt congenital heart disease with pulmonary hypertension (n=8). Three weeks after the establishment of the model, echocardiography, left and right cardiac catheter pressure measurement and lung histopathological staining were performed to compare the cardiac and pulmonary phenotypes of the rats. Results: Compared with the control group, there was no significant difference between the MCT group and the operation MCT group in the right ventricular hypertrophy, right ventricular dysfunction, mean pulmonary artery pressure, pulmonary vascular remodeling and other indicators 3 weeks after operation. But in many indexes related to left heart, the rats in the operation MCT group were significantly better than those in the simple MCT group. Compared with the control group, the left ventricular lumen diameter (LVID; d) and left ventricular ejection fraction (EF%) in the operation MCT group did not decrease in the diastolic period; The maximum rate of increase of right ventricular internal pressure (MAX dp/dt) and the maximum rate of decrease of left ventricular internal pressure (MIN dp/dt) in the operation MCT group were lower than those in the simple MCT group. Conclusion: Left to right shunt surgery can not change MCT-induced pulmonary hypertension and right heart remodeling, but can produce left heart compensation, which may be beneficial to the prognosis of patients. The animal model of this project establishes the basis for studying the different pathological mechanisms of idiopathic pulmonary hypertension and pulmonary hypertension associated with congenital heart disease.
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Monkeypox virus infection and the animal model of Monkeypox

bao rong

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Monkeypox is an infectious disease caused by Monkeypox virus （MPXV） infection. The host of MPXV remains unclear, and rodents and nonhuman primates consider the potential hosts. Monkeypox is rapidly spreading globally. However, the animal models for Monkeypox have not developed in the last decades in China. MPXV is a pathogen that seriously threat to human health. Its transmission among the population has presented new characteristics. Therefore, this article describes the discovery of MPXV and the early epidemic, different types of infection and co-infection. In addition, the experimental infection and animal models for Monkeypox in rodents and nonhuman primates were expounded in this paper.
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The expression of IGHG1 in acute myeloid leukemia THP-1 cell and the influences on cell proliferation, apoptosis and invasion by regulating TGF-β/Smad pathway

Lichangmei, Qiuli

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Objective To investigate the expression of immunoglobulin γ-1 heavy chain constant region (IGHG1) in acute myeloid leukemia (AML) THP-1 cell and its influences on cell proliferation, apoptosis and invasion by regulating the transforming growth factor β (TGF-β)/Smad pathway. Methods The bone marrow specimens of 9 children with AML, the bone marrow specimens of 8 children with fracture,human bone marrow stromal cells HS-5 and human AML cells THP-1, HL60 were used as research objects,Western Blot was used to detect IGHG1 protein expression; THP-1 cells were divided into: blank group (cells without any treatment), si-NC group, si-IGHG1-1 group, si-IGHG1-2 group, si-IGHG1-3 group, TGF-β group,si-IGHG1-1 TGF-β group,si-IGHG1-1 TGF-β LY364947 group, CCK-8 method was used to detect cell proliferation; apoptosis was detected by flow cytometry; Transwell experiment was used to detect cell invasion ; Western blot was used to detect the protein expression of IGHG1, TGF-β, p-Smad2, and p-Smad3 in each group of cells. Results Compared with the bone marrow of children with fracture, the expression level of IGHG1 protein [(0.24?.03) vs (0.87?.12] in the bone marrow of children with AML was significantly higher (P<0.05); compared with HS-5 cell, the expression level of IGHG1 protein in human AML cells THP-1, HL60 was significantly increased [(0.89?.14)(0.75?.08) vs (0.21?.02)] (P<0.05); compared with the blank group , the OD450 value (24, 48, 72h) of THP-1 cells, the number of invaded cells, and the protein expression of TGF-β, p-Smad2, and p-Smad3 were significantly reduced in the si-IGHG1-1 group, and the apoptosis rate was increased (P<0.05), while the corresponding indexes in TGF-β group were opposite (P<0.05); the TGF-β reversed the effects of silencing IGHG1 on the proliferation, apoptosis and invasion of THP-1 cells; compared with si-IGHG1-1 TGF-β group, TGF-β, p-Smad2, p-Smad3 protein, OD450 values (24, 48, 72 h) and invasion number of cells decreased significantly in si-IGHG1-1 TGF-β LY364947 group, and the cell apoptosis rate was increased (P<0.05). Conclusions IGHG1 is highly expressed in AML cells. Silencing IGHG1 can inhibit the proliferation and invasion of AML cells, and promote the apoptosis of AML cells. This mechanism may be related to the inhibition of TGF-β/Smad pathway.
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The relationship between atmospheric pollutants and some adverse pregnancy outcomes

jinjian, Chang Hui, Huang Hehuan, Peng Rui, Zhang Xiaoan

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With the rapid development of China's economy and the continuous acceleration of urbanization, the problem of air pollution is becoming increasingly prominent, which has a great impact on human health. In recent years, a large number of research work has emerged both domestically and internationally, and research results have shown a certain correlation between exposure to atmospheric pollutants during pregnancy and adverse pregnancy outcomes. The impact of air pollution on the health and embryonic development of pregnant women has received more attention. This article mainly provides a brief review on the impact of atmospheric pollutants on some adverse pregnancy outcomes and their possible biological mechanisms.
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Research Progress on Model Organism Zebrafish in Neurodegenerative Diseases

Huang Kongli, Su Shijie, Wang Yuting, LIU ZHUANGZHUANG, CAO DANDAN, WANG PEI, CHEN GUANLIN, Wang Qi

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Neurodegenerative disease （NDD）is a chronic and progressive neurological disease characterized by the loss of a large number of specific neurons. It mainly includes Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and amyotrophic lateral sclerosis (ALS). Although the lesions and etiologies of different types of neurodegenerative diseases are different, delayed neurodegenerative lesions and cell loss in specific brain areas are their common characteristics. For this reason, it is collectively referred to as neurodegenerative diseases. In recent years, zebrafish have attracted increasing attention from society as a new type of model organism. Although there are some differences between zebrafish and human central nervous systems, zebrafish neural conduction systems, neuronal and glial cell types, and disease-related gene homology are very similar to those of humans. Zebrafish has been widely used in the study of neurodegenerative diseases, and some achievements have been made in this field to improve our understanding of these diseases, but because of the complexity, multi-factors and multi-gene regulation of neurodegenerative diseases, the etiology and pathogenesis of zebrafish are not clear, so the treatment of this kind of disease has always been a difficult problem. By consulting relevant literature from home and abroad in recent years, this study reviews recent advances in neurodegenerative diseases using zebrafish as a model organism.
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Progress in irisin and its upstream and downstream antidepressants

Sangjiala, Lishanshan, Cuixin, Renqingqing, Houruiling, Panxingfang, Wangshenjun, Zhao

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Depression is the main cause of disability, and the adverse effects on people are difficult to eliminate. Despite the increasing number of antidepressants, depression is still not adequately treated clinically, and new mechanisms still need to be explored. As the beneficial effects of irisin on the nervous system are gradually elucidated, studies have found that irisin has an antidepressant effect, and irisin may become a new target for the treatment of depression. This study aims to explore the mechanism of irisin and its upstream and downstream antidepressants, by reviewing the existing studies to explain the link between depression and irisin, propose the potential mechanism of SIRT1 / PGC-1α mediating FNDC5/Irisin to regulate BDNF and promote neurogenesis to improve depression, and provide a new idea for the study of irisin and its upstream and downstream antidepressants.
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Advances of CREB in the regulation of memory through synaptic plasticity and its relation with Alzheimer’s disease

Luo Zhuohui, pang shuo, Zhang lianfeng

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Alzheimer’s disease is an irreversible heterogeneous neurodegenerative disease. AD patients are featured with memory loss and impaired synaptic plasticity. With a view to cAMP responsive element-binding protein which is intimately associated with synaptic plasticity. this assay summarized progress on the structure, signal pathway, downstream genes and relative memory regulation. The involvement of CREB in AD development would serve as references for AD researches based on synaptic plasticity improvement.
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Research progress on the regulation of lymphangiogenesis and its role in myocardial infarction

duqing, wanghe

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Lymphatic system plays an important role in regulating interstitial fluid homeostasis, lipid metabolism and immune function. After myocardial infarction, enhanced lymphangiogenesis accelerates the clearance of infiltrating immune cells, reduces the production of pro-inflammatory cytokines, reduces edema, inflammation, and fibrosis, and promotes the recovery of damaged heart function. Vascular endothelial growth factor-C (VEGF-C) and its receptor VEGFR-3 are components of the lymphangiogenesis pathway and play a critical role in maintaining tissue fluid balance and myocardial function after cardiac injury. Lymphatic vessels are closely related to the immune system. Different immune cell groups can stimulate or inhibit lymphatic remodeling. Macrophages are congenital immune cells widely distributed in organs and tissues, and play an important role in various physiological and pathological processes such as organ development, host defense, acute and chronic inflammation, tissue homeostasis and remodeling. More mechanisms of lymphangiogenesis need to be identified to provide effective targets for clinical stimulation of lymphangiogenesis to treat heart disease. This paper reviews the basic pathological changes of the heart and lymphatic vessels after myocardial infarction, the regulatory factors of lymphangiogenesis, and the influence of macrophages on lymphangiogenesis.
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Effects of LncRNA FGD5-AS1 targeting and regulating miR-129-5p on the proliferation, apoptosis, migration and invasion of oral squamous cell carcinoma cells

Yangfeng, Liuguanglong

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Objective To investigate the effects of long non-coding RNA (LncRNA) FGD5-AS1 on the proliferation, apoptosis, migration and invasion of oral squamous cell carcinoma (OSCC) cells through targeted regulation of miR-129-5p. Methods The expression of FGD5-AS1 in OSCC was analyzed by online database. The tumor tissues, normal tissues, and the human oral mucosal cells (HOK) and OSCC cells (SCC-9, HSC-4, SCC-25, CAL-27) cultured in vitro from 30 OSCC patients collected in our hospital were used as research subjects, qRT-PCR method was performed to detect the expression of FGD5-AS1 and miR-129-5p. The CAL-27 cell line with the highest FGD5-AS1 expression was randomly separated into Control group (normal culture, no transfection), si-NC group (transfected with si-NC), si-FGD5-AS1 group (transfected with si-FGD5-AS1), si-FGD5-AS1 NC inhibitor group (co-transfected with si-FGD5-AS1 and NC inhibitor) and si-FGD5-AS1 miR-129-5p inhibitor group (co-transfected with si-FGD5-AS1 and miR -129-5p inhibitor), CCK-8 method and clone formation assay were used to detect the proliferation ability of CAL-27 cells; the apoptosis level of CAL-27 cells was detected by flow cytometry; the migration ability of CAL-27 cells was detected by wound-healing assay; Transwell chamber was used to detect the invasion ability of CAL-27 cells; and dual luciferase reporter experiment verified the targeting relationship between FGD5-AS1 and miR-129-5p; the expression of high mobility group protein B1(HMGB1) was detected by Western blot. In vivo xenograft tumor model was constructed and divided into sh-NC group, sh-FGD5-AS1 group, miR-129-5p inhibitor group, and sh-FGD5-AS1 miR-129-5p inhibitor group. Tumor volume and tumor were detected. QRT-pcr was used to detect the expression of FGD5-AS1 and miR-129-5p in transplanted tumor tissues. The expression of HMGB1 and Ki67 was detected by immunohistochemistry. Results Database analysis showed that the expression level of FGD5-AS1 in OSCC tumor tissues was 4 times higher than that in normal tissues, and FGD5-AS1 expression was associated with poor grade in OSCC patients. Compared with normal tissues or human oral mucosal cells, the expression of FGD5-AS1 in tumor tissues and OSCC cell lines was significantly increased, and the expression of miR-129-5p was significantly decreased (P<0.05), the CAL-27 cells with the highest expression level of FGD5-AS1 were selected for transfection experiments. Compared with the Control group and the si-NC group, the apoptosis rate of the si-FGD5-AS1 group was significantly increased, and the OD value (48 h, 72 h, 96 h), scratch healing rate and the number of invaded cells were significantly reduced (P<0.05). MiR-129-5p was the target gene of FGD5-AS1. Inhibiting the expression of miR-129-5p was able to reverse the effects of interference FGD5-AS1 on the proliferation, apoptosis, migration and invasion of OSCC cells, thereby restoring the cancer-promoting effect of FGD5-AS1. After FGD5-AS1 was disrupted, HMGB1 expression was down-regulated by significantly enhancing miR-129-5p expression (P<0.05). In vivo experiments showed that FGD5-AS1 silencing significantly inhibited the growth and expression of HMGB1 and Ki67 (P<0.05), inhibition of miR-129-5p was the opposite; Inhibition of miR-129-5p reversed the inhibition of FGD5-AS1 on tumor growth and expression of HMGB1 and Ki67 (P<0.05). Conclusions FGD5-AS1 is up-regulated in OSCC cells. Interfering with FGD5-AS1 can inhibit proliferation, migration and invasion of OSCC cells and promote apoptosis by targeting miR-129-5p / HMGB1 axis.
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Behavioral assessment in the parkinson’s model of nonhuman primates

liushuyi, zhengbo wang

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Parkinson's disease is a neurodegenerative disease, can cause a series of patients with symptoms of movement and the movement, behind the pathogenesis is unclear, to explore the mechanism behind these phenotypic requires an appropriate animal model of rodents in the movement and the movement is very difficult to accurately simulate the patient symptoms, causes related to preclinical studies have limitations, in translational medicine. Non-human primate animal models can make up the gap between rodents and humans, thus the non-human primate PD model of movement and the movement symptoms, is very important to research on mechanism and therapy, this review summarizes the different behavior in quantitative way, and compared the advantages and disadvantages between different methods, for studying the PD monkey model provides a behavioral testing for help.
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Advances in the construction of animal models of severe asthma

Wei Dandan, Wang Liting, Long Jie, Chen Yanjiao, Wang Yu, Yang Yongqing, Xu Yudong

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Severe asthma (SA), which requires high doses of glucocorticoids in combination with other medications to maintain symptom control or is uncontrollable even with these treatments, is currently a challenge in the clinical management of asthma. The establishment of a stable and reproducible experimental animal model that highly mimics the pathophysiological and clinical characteristics of patients with severe asthma is a key fundamental link in deepening the study on the pathogenesis of severe asthma, identifying potential therapeutic targets and developing targeted drugs. This paper reviews the experimental studies related to the construction of animal models of severe asthma in the past 10 years, and summarizes the recent progress in the establishment and evaluation of animal models of severe asthma from three aspects: animal selection, animal model construction protocols, and model pathological phenotypes. To summarize and analyze the latest progress in the construction of SA animal models, and provide a reference for SA basic research based on animal models.
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Research progress in experimental models of pulmonary arterial hypertension

xiejincheng, Chenjianying, Dengshaodong, Xiao mengyuan

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Pulmonary hypertension is a chronic progressive disease that, if not treated promptly, can ultimately lead to right heart failure and even death In order to explore the pathogenesis of pulmonary arterial hypertension and find more effective treatment methods, it is necessary to establish a suitable experimental model. In this paper, Pubmed, CNKI and other databases were used to search relevant literature, and the preparation methods and research progress of various experimental models of pulmonary arterial hypertension in recent years were summarized. The preparation methods of the models were classified to show the pathological characteristics of the disease more directly. On this basis, the present situation and existing problems of the in vitro and in vivo model of pulmonary arterial hypertension were discussed, in order to provide reference for the pathogenesis and clinical research of pulmonary arterial hypertension.
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Research progress of experimental premenstrual dysphoria model in rodents

xujialing

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Premenstrual dysphoric disorder (PMDD) is a subtype of Premenstrual syndrome with high prevalence in women during their reproductive life. It includes physical symptoms such as breast tenderness, headache as well as serious emotional symptoms such as anxiety, depression and irritability. These symptoms are menstrual specific, they appear before menstruation and disappear within a week after it ends. PMDD threatens the health of female patients all over the world, In The Diagnostic and Statistical Manual of Mental Disorder(Fifth edition ed,DSM-5）, PMDD is identified as one of the five types of depression. At present, studies on the pathological mechanism of PMDD mainly focus on hormone and receptor expression, which is the theoretical basis of the animal model establishment, as well. Animal model that can model after clinical symptoms of human beings is a very important to connect basic research to clinical research, which is also crucial to explore the pathogenesis and develop appropriate drugs. Although many kinds of animal models of PMDD have been used in experimental studies, there are still many limitations, which resulting in a barrier to further investigation of PMDD. Therefore, this review arranged the known pathogenesis research of PMDD and discuss the existing animal models of PMDD, aims to provide reference for PMDD related mechanism research and drug development.
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Analysis of animal models of keratitis based on the characteristics of clinical conditions of traditional Chinese and Western medicine

nanshuo

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Abstract: Keratitis is a common ophthalmic disease with a high rate of blindness. This paper reviews a large number of relevant literature of animal models of keratitis, summarizes and analyzes the mechanism of existing animal models of keratitis, and evaluates the clinical anastomosis degree of traditional Chinese and Western medicine in combination with the established clinical diagnostic standards of traditional Chinese and Western medicine, analyzes its advantages and disadvantages, and puts forward some suggestions. It is found that most of the existing models are based on Western medical theories, and lack the diagnostic standards of traditional Chinese medicine. The model is mostly modeled by a single factor, which cannot well simulate the real lesion process of the disease; The diagnosis of the model lacks apparent indicators; It is recommended that animals be modeled by combining disease evidence. It is very important to prepare animal models of keratitis with high clinical compatibility and establish perfect evaluation standards, which can help us better understand the occurrence and development of keratitis in modern medical experiments, and effectively prevent and treat it.
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Study on the uptake and transport properties of euscaphic acid in Caco-2 cell model based on UPLC-TQ-MS

wangning, xieli, ding wenhuan, tian li

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ABSTRACT: Objective Caco-2 cell model was established to explore euscaphic acid uptake and transport mechanism in this study. Methods Ultra-high performance liquid chromatography-triple quadrupole-mass spectrometry(UPLC-TQ-MS) was employed to determine the content of euscaphic acid. The effects of different time and temperature on its uptake were investigated. Based on the results of the uptake studies, the effects of different concentrations, P-gp inhibitors, chelating agents and pH values on its bidirectional transport were explored. Results The uptake of euscaphic acid was (8.38 ?0.87) μg穖g-1 for 180 min on the Caco-2 cell model at 37 癈. The apparent permeability coefficient (Papp values) of euscaphic acid for low, medium and high concentrations were(61.41 ?.92)?0-4、(146.90?4.91)?0-4 and (167.18?.72)?0-4 cm穝-1 respectively, which were positively correlated with the concentrations. P-gp inhibitors and chelating agents had no effect on its Papp values. Weakly acidic environment (pH6.00) significantly increased its Papp value, and the efflux rate (ER) ranged from 0.8–1.4. Conclusion The above results indicate that euscaphic acid has good transmembrane permeability in Caco-2 cell model, and the uptake mode is mainly passive diffusion. It is not a substrate of P-gp and there is no cellular bypass transport. This research may provide an experimental basis for the in vivo intestinal absorption of medicines containing euscaphic acid.
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Mechanism of taxifolin regulating endoplasmic reticulum stress PERK-ATF4 pathway to reduce myocardial hypertrophy in hypertensive rats

yujinyu, hanjing, zhangying, yuwen

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【Abstract】 Objective To investigate the impact and molecular mechanism of taxifolin (TAX) on myocardial hypertrophy in spontaneously hypertensive rats (SHR). Methods Twenty-four SHRs were separated into SHR control group (SHR group), TAX group (20 mg/kg), and TAX PERK activator CCT020312 (CCT) group (20 mg/kg TAX 2 mg/kg CCT), 8 per group; another 8 normal blood pressure Wistar-Kyoto (WKY) rats were regarded as the normal control group (WKY group), and all were given corresponding drugs for 8 weeks of continuous intervention. During the experiment, the changes in blood pressure of the rats were observed, and after the intervention, the thickness of the diastolic ventricular septum (IVSd), the thickness of the systolic ventricular septum (IVSs), and the left ventricular ejection fraction (LVEF) were detected by echocardiography to determine the degree of myocardial hypertrophy and cardiac function, then the cardiac index and left ventricular index were calculated, hematoxylin-eosin (HE) staining, wheat germ agglutinin (WGA) staining and Masson staining were performed to evaluate the pathological changes of myocardial tissue, real-time quantitative PCR (qRT-PCR) was performed to detect the expressions of atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), type I collagen α1 chain (COL1A1) and type III collagen α1 chain (COL3A1) mRNA in myocardial tissues, Western blot was performed to detect the expressions of protein kinase R-like endoplasmic reticulum kinase (PERK)-activator of transcription 4 (ATF4) pathway-related proteins in cardiac muscle. Results After the intervention, compared with the WKY group, the systolic blood pressure (SBP), diastolic blood pressure (DBP), IVSd, IVSs, cardiac index, left ventricular index, myocardial cell cross-sectional area, collagen volume fraction (CVF), myocardial tissue ANP, BNP, COL1A1 and COL3A1 mRNA expressions, glucose-regulated protein 78 (GRP78), ATF4, C/EBP homologous protein (CHOP) protein levels and p-PERK/PERK ratio in the SHR group increased (all P<0.05), LVEF decreased (P<0.05); compared with SHR group, the SBP, DBP, IVSd, IVSs, cardiac index, left ventricular index, myocardial cell cross-sectional area, CVF, myocardial tissue ANP, BNP, COL1A1 and COL3A1 mRNA expressions, GRP78, ATF4, CHOP protein levels and p-PERK/PERK ratio in TAX group decreased (all P<0.05), LVEF increased (P<0.05); CCT020312 partially reversed the protective effects of TAX on cardiac function and cardiac hypertrophy. Conclusion TAX can improve hypertensive myocardial hypertrophy by inhibiting endoplasmic reticulum stress (ERS), and its mechanism may be related to inhibiting PERK-ATF4 pathway.
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Study on tissue distribution difference of ligustrazine-Salvia miltiorrhiza before and after compatibility in acute myocardial ischemia model rats

lirong, goujian, liuting, gongzipeng, luyuan, liuchunhua, hunagyong, sunjia

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Objective To investigate the difference in tissue distribution of ligustrazine hydrochloride and Salvia miltiorrhiza (Danshen) in Acute myocardial ischemia (AMI) rats. Methods AMI model was induced by subcutaneous injection of isoproterenol hydrochloride. UPLC-MS/MS method was used to determine the content differences of ligustrazine and danshensu in heart, liver, spleen, lung, kidney and brain tissues after single intravenous injection of Danshen injection (DGI), Ligustrazine injection (CGI) and Shenxiong glucose injection (SGI) at different time points. Results After intravenous injection, ligustrazine and danshensu were widely distributed in tissues of AMI rats and reached their peak rapidly. Before and after compatibility, the content of ligustrazine was the highest in brain tissue and the lowest in liver tissue. The content of danshensu in kidney tissue was the highest, and in brain tissue was the lowest, indicating that ligustrazine could penetrate the blood-brain barrier more easily than danshensu, and the main accumulation tissues were different. The AUC of ligustrazine and danshensu in the heart of the target organ was significantly increased (P < 0.001). Conclusion It is speculated that the combination of ligustrazine and salvia miltiorrhiza may enhance the therapeutic effect by increasing the distribution of main pharmacodynamic components in the heart, so that SGI can play a better role.
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The role of PI3K/Akt/mTOR signaling pathway in the pathogenesis of TRALI rats

liushuangchun, Zhang Xijiang, Chen Zaihuan, Wang Luqian, Lin Hairong

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Objective: To study the effect of PI3K/Akt/mTOR signaling pathway on the pathogenesis of TRALI. Methods: Animal model was established by the method of trauma-blood loss-massive transfusion, and the pulmonary histopathological changes were detected by HE staining to determine whether the rats had pulmonary edema. The protein and mRNA expression levels of TNF-α, IL-6 and IL-1β in peripheral blood or lung tissues in TRALI rat models were detected by ELISA and qRT-PCR. The expression levels of PI3K/Akt/mTOR signaling pathway related proteins and apoptosis-related proteins Bax, Bcl-2 and Caspase3 were detected by western blotting. Results: Alveolar tissue structure was seriously damaged, the alveolar wall was thickened, there was pink edema fluid in the alveolar cavity, inflammatory cells infiltrated, edema was obvious in TRALI model rat. The expression levels of inflammatory cytokines TNF-α, IL-6 and IL-1β were significantly increased in peripheral blood and lung tissues (P<0.05); PI3K/Akt/mTOR signaling pathway was activated, the expression of p-mTOR/mTOR was significantly increased, and the expression of apoptotic protein Bax and Caspase 3 was inhibited, and the expression of anti-apoptotic protein Bcl-2 was increased (P<0.05). Conclusion: As a potential drug target, mTOR is an important means for clinical prevention and control of the occurrence and development of TRALI by defining the exact time target of its protective and damaging effects and selecting the optimal time of medication due to its complicated mechanism.
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Alterations of Gut Microbiota - Short Chain Fatty Acid Axis in IBS-D Rats and the Effect of Sodium Butyrate

zhan kai, Wu haomeng, zheng huan, qin shumin, Huang shaogang, yang yuanming

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Objective To explore the alterations of gut microbiota - short chain fatty acid metabolic axis in IBS-D rat model, and to explore the effect of sodium butyrate on this axis. Methods Seventeen Wistar rats were randomly divided into three groups. The IBS-D rat model was induced by 4% acetic acid enema combined with restraint stress. During the modeling period, sodium butyrate was injected intraperitoneally. The fecal flora of rats was detected by 16sRNA technology, and the fecal short chain fatty acid content of rats was detected by liquid chromatography mass spectrometry (LC-MS). Results Compared with the normal group, the weight of the model group was decreased, AWR score and fecal water content have a significant increase, the relative abundance of intestinal probiotics was decreased，while that of g-Blautia was elevated, the fecal acetic acid content was increased significantly, and the contents of butyric acid and valeric acid was decreased significantly in the model group. After drug intervention, compared with the model group, the weight of rats in the sodium butyrate group was increased, the AWR score and fecal water content was decreased significantly, the relative abundance of g-Blautia was decreased significantly, and the fecal butyric acid and valeric acid content was obviously increased. Conclusions Sodium butyrate can alleviate diarrhea and colon visceral hypersensitivity in IBS-D rats by improving the imbalance of gut microbiota - short chain fatty acid metabolic axis.
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Advances in Ferroptosis-Based Therapy for Aging and Aging-Related Diseases

Zhou yongchang, Tao Siman, Chen Shengqiang, Pu Xiuying

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Ferroptosis is a novel form of programmed cellular necrosis proposed in recent years, which is found in various diseases and seriously impacts on human health. Numerous studies have shown that inhibition or promotion of ferroptosis can improve many aging and aging-related diseases, and Traditional Chinese medicine plays an important role in this regard. This paper reviews the effects and mechanisms of Ferroptosis on aging and aging-related diseases, and compares the research progress of TCM in the treatment of ferroptosis-mediated aging and aging-related diseases in recent years, aiming to provide more options for the treatment and prevention of aging and aging-related diseases.
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Research progress in the pathogenesis of inflammatory bowel disease

Houxiaoting, Menghuan, Xuejiachen, Zhanghuamin, Wangkesi, Wangxude

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Inflammatory bowel disease (IBD) is a global idiopathic disease, involving the ileum, rectum and colon. IBD begins to appear early in clinical symptoms, including abdominal discomfort, diarrhea, hematochezia, fever, fatigue and weight loss. The diagnosis of IBD is based on the comprehensive evaluation of relevant clinical manifestations, endoscopic examination results and histopathological characteristics of pathological tissue specimens. Biological agents, oral corticosteroids, salicylic acid and surgery are the main conventional treatments for IBD. In recent years, considerable progress has been made in elucidating the pathogenesis of IBD. In clinical practice, it is considered that the complex interaction between genetic susceptibility, environmental factors and intestinal mucosal barrier leads to abnormal oxidative stress, autophagy and mucosal immune response. This paper briefly summarizes and expounds the research progress of genetic and environmental factors, intestinal mucosal barrier function, oxidative stress, autophagy dysfunction and adaptive immune response, so as to provide basis for further research and development of treatment methods and improvement of clinical treatment effect.
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Effect of Bushen Jianpi Kaixin formula on autophagy and apoptosis in AD rats

li ying, Wang Ying, Kong Mingwang

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Objective To investigate the effects of Bushen Jianpi Kaixin Formula (BSJPKXF) on the learning and memory ability of Alzheimer s disease (AD) model rats and the related autophagy and apoptosis in cortex of AD model rats, and exploring the underlying mechanism of BSJPKXS. Method The 60 eligible rats were randomly divided into six groups (n = 10): control group, AD group, Bushen group (BS, 3.6g/kg·d), Jianpi group (JP, 4.05g/kg·d), Kaixin group (KX, 2.34g/kg·d) and Bushen Jianpi Kaixin group (BSJPKX, 9.99g/kg·d). AD mouse model was established by intraperitoneal injection of D-gal. The rats in BS group, JP group, KX group and BSJPKX group were gavaged with corresponding drugs once a day. The rats in control group and AD group were treated with equal amount of normal saline one time per day. After four weeks, the learning and memory ability was tested by Morris water maze. The open-field test was used for detecting the cognitive function in rats. The expression of LC3-I, LC3-II and Beclin in cerebral cortical tissues were detected by western bolt. The expression of Bax and Bcl-2 in cerebral cortical tissues were detected by immunohistochemistry. The related mRNA level of Beclin 1, P62, Bax and Bcl-2 in cerebral cortical tissues were detected by RT-PCR. Result Compared with the control group, D-gal significantly decreased the spatial learning and memory ability of rats in the AD group (P < 0.01), decreased the expression of Beclin, LC3-I/LC3-II, Bcl-2 and Bcl-2/Bax, increased the mRNA level of P62 and the expression of Bax (P < 0.01). After treatment, related to the AD model group, Bushen Jianpi Kaixin formula improved the spatial learning memory ability of rats in the BSJPKX group (P < 0.01), increased the expression of Beclin, LC3-I/LC3-II, Bcl-2 and Bcl-2/Bax, decreased the mRNA level of P62 and the expression of Bax (P < 0.01). Conclusion Bushen Jianpi Kaixin formula can improve cognitive impairment in AD rats. The mechanism is presumedly related to the reduction of neural autophagy and apoptosis.
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The evaluation of experimental animal studies on acupuncture for hypertension based on the SYRCLE’s tool and the ARRIVE guidelines

Tang wenjing, ZHANG Yue, LI Yuxi, ZHONG Dongling, JIN Rongjiang, ZHANG Lili, LI Juan

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Objective To evaluate the risk of bias and reporting quality of animal experimental studies on acupuncture for hypertension, and analyze the deficiencies in experimental design, implementation and reporting, so as to decrease the risk of bias of researches and improve the reporting quality of animal studies. Methods Databases including China national knowledge infrastructure（CNKI）, Wanfang database（WANFANG）, Chinese science and technology periodical database（VIP）, Chinese biomedical literature database（CBM）, Web of Science, PubMed, Embase, and The Cochrane Library were searched from inception to October 8, 2022. Two researchers independently screened experimental studies related to acupuncture interventions in hypertensive animals according to eligibility criteria. The SYRCLE’s tool and the ARRIVE guidelines 2.0 were used to evaluate the risk of bias and reporting quality of the included literature. Excel 2019 was used to extract data and descriptive analysis was conducted according to the results. Results A total of 79 animal experiments on acupuncture for hypertension were included, among which 16 and 21 were published in Chinese core journals and science citation index（SCI）journals respectively. The result of SYRCLE’s tool showed that 5 of the 10 items were evaluated as well, while the rest were unclear risk or high risk of bias. Of the 79 included articles, the risk of bias of 19 articles were low, while the remaining studies had some risk of bias. The results of the ARRIVE guidelines 2.0 indicated that 19 of the 38 sub-items were well reported, while the rest were poorly reported.The reporting quality of 51 articles were good and the remaining studies were inadequately reported. Conclusions At present, the risk of bias of acupuncture intervention in hypertensive animal experiments is high and the reporting quality is generally low. The inadequate description of some important entries had impact on the reproducibility of the experiments and the translation of the results.The SYRCLE’s tool and ARRIVE guidelines 2.0 are recommended to be used as reference during experimental design and reporting, thus improving the standardization and reporting quality of acupuncture for hypertensive animals.
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Autophagy: the key mechanism of exercise in improving neurodegenerative diseases

Chen Xianghe, Qiu Xiao, Liu Chi, Shen Ziming, Zhou Xiangxiang

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Autophagy regulation of neurological diseases is the focus of current research in the field of neuroscience. Autophagy disorder leads to protein expression, deposition and dysfunction such as Aβ、Tau、α-syn and causes neurodegenerative diseases such as AD, PD and HD. Exercise is an important means to improve neurodegenerative diseases, which is closely related to the up-regulated expression of LC3, Beclin-1, Lamp1 and other autophagic factors after the activation of AdipoR1/AMPK/TFEB, AMPK/mTOR and other pathways. Higher autophagy level can remove the deposition of Aβ、Tau、α-syn and other proteins in the brain and can improve the neurodegeneration, synaptic structure and function disorder caused by neurodegenerative diseases. This study reviewed and analyzed the mechanism of autophagy in the improvement of neurodegenerative diseases by exercise, which will provide a solid theoretical basis and new research ideas for the improvement of neurodegenerative diseases by exercise.
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guojia

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Editor Sun

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Research advances of trophoblast cells in threatened abortion complicated with intrauterine hemorrhage

HuoYan, Zhu Jun nan, Fu Ya qi, Chen Ping, Xu Guang li

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Threatened abortion complicated with intrauterine hemorrhage is a common disease during pregnancy.Its pathogenesis is related to the imbalance of maternal-fetal interface microenvironment and the obstruction of uterine spiral artery remodeling. Trophoblast cells are the outermost layer of the maternal-fetal interface microenvironment .Its proliferation, migration and invasion are closely related to normal pregnancy.It plays an irreplaceable role in immune tolerance and regulation, uterine spiral artery remodeling, and maintenance of maternal-fetal interface microenvironment.In recent years, trophoblast cells have become the main line of research in autoimmune diseases and other fields.Studies have found that it plays an important role in the diagnosis and treatment of threatened abortion complicated with intrauterine hemorrhage.This article reviews the research progress of trophoblast in the treatment of threatened abortion complicated with intrauterine hemorrhage.
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SUNYE

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yiyi

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Volume 33,2023 Issue 9

Volume 33,2023 Issue 9

Volume 33,2023 Issue 9

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