Abstract: Objective 　The prognosis of patients with left-to-right shunt congenital heart disease-associated pulmonary hypertension is significantly better than that of patients with idiopathic pulmonary hypertension, but the specific mechanism is unclear. The purpose of this study was to establish 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 terms of pulmonary vascular remodeling and cardiac remodeling. Methods 　Male SD rats were divided into three groups: control group (n= 8), monocrotaline (MCT) group (50 mg/ kg) to simulate idiopathic pulmonary hypertension (n= 8), and cervical arteriovenous shunt surgery+monocrotaline (MCT) group (50 mg/ kg) to simulate left-to-right shunt congenital heart disease with pulmonary hypertension (n= 8). Three weeks after establishment of the model, echocardiography, left and right cardiac catheter pressure measurements, and lung histopathological staining were performed to compare cardiac and pulmonary phenotypes of the rats. Results 　Compared with the control group, no significant difference was found between the MCT and the operation+MCT groups in terms of the right ventricular hypertrophy, right ventricular dysfunction, mean pulmonary artery pressure, pulmonary vascular remodeling, or other indicators at 3 weeks after the operation. However, many indexes related to left heart in rats of the operation+MCT group were significantly better than those in the simple MCT group. Compared with that in the control group, the left ventricular lumen diameter (and left ventricular ejection fraction) in the operation+MCT group did not decrease in the diastolic period. The maximum rate of increase in right ventricular internal pressure and the maximum rate of decrease in left ventricular internal pressure in the operation+MCT group were lower than that in the simple MCT group. Conclusions　Left-to-right shunt surgery cannot change MCT-induced pulmonary hypertension or right heart remodeling, but can produce left heart compensation, which may be beneficial to the prognosis of patients. The animal model of this study establishes the basis to examine various pathological mechanisms of idiopathic pulmonary hypertension and pulmonary hypertension associated with congenital heart disease.

Abstract: Objective 　We studied the effect and mechanism of acupoint catgut embedding on rheumatoid arthritis (RA) by regulating the PD-1/ OX40 signaling pathway. Methods 　Twenty-five SD female rats were treated with complete Freund’ s adjuvant to establish the RA model. Rats were divided into control, model, Leflunomide, acupoint catgut embedding, and acupoint catgut embedding + Leflunomide groups. The degree of inflammation was determined by the arthritis index. Serum interleukin 6 (IL-6) and interleukin 8 (IL-8) levels were measured by ELISA. HE staining was used to observe infiltration of synovial inflammatory cells, synovial tissue, fibrous tissue, macrophage proliferation, and angiogenesis. Proportions of PD-1/ OX40 and CD4⁺ CD28⁺cells were determined by flow cytometry. Results　Except for the control group, rats in each group had erythema and moderate swelling from the ankle joint to the metatarsal bone or palm joint. After 14 days, the scores of the model group did not change significantly. Scores of inflammatory factors in the catgut embedding + Leflunomide group began to decrease, and those in the acupoint catgut embedding + Leflunomide group decreased the fastest. Serum levels of IL-6 and IL-8 in the model group were significantly increased (P<0. 01), whereas serum levels of IL-6 and IL-8 in Leflunomide, acupoint catgut embedding, and acupoint catgut embedding + Leflunomide groups were significantly decreased (P<0. 01). The synovial tissue of model group rats was damaged with a large amount of inflammatory cell infiltration, vascular dilation, and fibrous cell proliferation. After treatment with leflunomide and acupoint catgut embedding, inflammatory cell infiltration in synovial tissue was significantly reduced and vascular proliferation was inhibited. The effect was most significant when leflunomide and acupoint catgut embedding were combined. In the model group, PD-1 expression was increased, while OX40 expression was significantly reduced (P<0. 01). CD4 and CD28 expression was significantly increased (P<0. 01). OX40 expression was significantly increased in Leflunomide, acupoint catgut embedding, and acupoint catgut embedding + Leflunomide groups, while CD4, CD28, and PD-1 expression was significantly decreased (P<0. 01). Conclusions　Acupoint catgut embedding improves RA symptoms and has a combined therapeutic effect with leflunomide. Its mechanism may be related to the PD-1/ OX40 signaling pathway.

Abstract: Objective 　To investigate the improving effect of modified Chaihu Guizhi Decoction (CGD) on osteoporosis rats by regulating the Wnt/ β-catenin signaling pathway. Methods 　SD rats were assigned to Model, CK, high-dose CGD (CGD-H; 20 g/ kg), low-dose CGD (CGD-L; 5 g/ kg), and estradiol valerate (EV; 9 mg/ kg), Wnt/ β- catenin pathway inhibitor (DKK-1, 100 mg/ kg), and CGD-H+DKK-1 (20 g/ kg+100 mg/ kg) groups with 12 rats per group. Except for those in the CK group, rats were administered 70 mg/ kg retinoic acid to establish the osteoporosis(OP) model, and rats in the CK group were administered the same amount of normal saline. From week 4 of modeling, the corresponding drug was administered for 4 weeks. ELISA were applied to measure serum levels of collagen type I C-terminal peptide (CTX-Ⅰ) and osteocalcin (BGP). Changes in the bone volume fraction, bone trabecular thickness, bone mineral density, and bone trabecular number were observed. HE staining was applied to assess pathological changes in the rat femur. Alkaline phosphatase (ALP) calcium-cobalt staining was applied to detect osteoblast activity in the rat femur. Osteoclast activity in rat femur tissue was detected by tartrate-resistant acid phosphatase (TRAP) staining. Western blot was applied to detect Wnt3a and β-catenin proteins in femoral tissue. Results　Compared with the CK group, femoral tissue of the Model group had severe pathological damage, the CTX-Ⅰ level and osteoclast activity were increased, and the BGP level, bone volume fraction, bone trabecular thickness, bone mineral density, bone trabecular number, osteoblast activity, and Wnt3a and β-catenin protein expression were decreased (P< 0. 05). Compared with the Model group, pathological damage of the femur in CGD-L, CGD-H, and EV groups was alleviated, the CTX-Ⅰ level and osteoclast activity were decreased, the BGP level, bone volume fraction, trabecular thickness, bone mineral density, bone trabecular number, osteoblast activity, and Wnt3a and β-catenin protein expression were increased, and the opposite trends of the corresponding indicators were observed in the DKK-1 group (P<0. 05). Compared with the CGD-H group, femoral tissue of the CGD-H+DKK-1 group was severely damaged, the CTX-Ⅰ level and osteoclast activity were increased, and the BGP level, bone volume fraction, bone trabecular thickness, bone mineral density, bone trabecular number, osteoblast activity, and Wnt3a and β-catenin protein expression were decreased (P<0. 05). Conclusions　CGD may improve OP in rats by activating the Wnt/ β-catenin pathway.

Abstract: Objective 　To explore the role and possible mechanism of a disintegrin and metalloproteinase 10 (ADAM10) in osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and tibial fracture union. Methods 　BMSCs of SD rats were cultured, stably transfected with a negative control (NC) shRNA pGFP-V-RS vector, and divided into sh-NC and sh-NC+DMSO groups. BMSCs were stably transfected with an ADAM10 shRNA pGFP-V-RS vector and divided into sh-ADAM10, sh-ADAM10+DMSO, and sh-ADAM10+valproic acid (VPA) groups. After 14 days of osteogenic induction, absorbance at 405 nm after alizarin red staining, ALP activity, and ADAM10, OCN, Runx2, CoLI, NICD, and Hes1 expression levels were analyzed. A tibial fracture model was established in SD rats, and NC shRNA or ADAM10 shRNA pCMV5. 0 vectors were injected locally. Fracture healing and gene expression were then observed for 4 weeks. Results　The ADAM10 expression level in BMSCs of the sh-ADAM10 group was lower than that in the sh-NC group. After osteogenic induction, the absorbance value of alizarin red staining at 405 nm, ALP activity, and OCN, Runx2, CoL-I, NICD, and Hes1 expression levels of the sh-ADAM10 group were higher than those of the sh-NC group (P< 0. 05). The absorbance value of alizarin red staining at 405 nm, ALP activity, and OCN, Runx2, and Col-I expression levels of the sh-ADAM10+VPA group after osteogenic induction were lower than those in the sh-ADAM+DMSO group (P< 0. 05). Healing of the tibial fracture in the sh-ADAM10 group was better than that in the sh-NC group, and OCN, Runx2, CoL-I, NICD, and Hes1 expression levels were higher than those in the sh-NC group (P<0. 05). Conclusions　Knocking down ADAM10 expression promotes osteogenic differentiation of BMSCs and tibial fracture healing, which is related to inhibition of the Notch1 pathway.

Abstract: Objective To establish an efficient method to isolate and culture rat bone marrow mesenchymal stem cells (BMSCs) and apply PKH26 to label them in vitro to explore the effect of PKH26 labeling on their biological characteristics and achieve in vitro tracing. Methods 　Hind limb bones of 5-day-old rats were separated, surrounding muscle and fascia were removed, and the bones were cut into small pieces for culture. BMSCs were purified by fluid exchange and passaging. Cell surface antigens of third passage cells were analyzed by flow cytometry. Under the same culture conditions, third passage BMSCs were labeled with PKH26. Cell morphology and proliferation of labeled and unlabeled groups were observed under a fluorescence microscope. Adipogenic induction characteristics and identification of labeled and unlabeled groups were compared. Results　The bone marrow slice method was used to separate hind limb bones of 5-day-old mice. The BMSC shape was slender, spindle, and uniform. A large number of BMSCs was rapidly obtained in a short time. Flow cytometry showed CD29 expression in (91. 18± 1. 29) % of cells, CD90 expression in (95. 04 ± 0. 11)% of cells, and CD45 expression in (1. 74 ± 0. 36) % of cells. PHK26 labeling had no significant effect on the morphology or proliferation of BMSCs ( P> 0. 05) or induction of osteogenesis or adipogenesis. Conclusions A large number of high-purity BMSCs was rapidly cultured by the method from 5-day-old rat bone marrow slices, which can be used as seed cells for bone tissue engineering. PKH26 can also label rat BMSCs in vitro.

Abstract: Objective 　To investigate the effects of low doses of bisphenol A (BPA) and di (2-ethyl) hexyl phthalate (DEHP) on aldo-keto reductase 1C3 (AKR1C3) expression in adult SD rats. Methods 　Fifty-six adult male SD rats were randomly divided into seven groups (n =8 rats in each group) and administrated BPA (10, 30 and 90 μg/ kg, i. g. ), DEHP (30, 90 and 270 μg/ kg, i. g. ), or the vehicle once a day for 4 weeks. The animals were sacrificed on the day after the last treatment. Blood was collected, and prostate tissues were dissected and categorized into different lobes. Levels of AKR1C3 in serum and prostate were measured by an enzyme-linked immunosorbent assay, and AKR1C3 expression in each prostate lobe was analyzed by immunohistochemistry. Results　After BPA administration, AKR1C3 expression in the ventral prostate was increased, and a significant difference was found in the 90 μg/ kg group (P<0. 05). AKR1C3 protein expression in the dorsal prostate was increased, and a significant difference was found in the 10 μg/ kg group (P<0. 01, P< 0. 001). After DEHP administration, the serum level of AKR1C3 in the 270 μg/ kg group was significantly higher than that in the control group (P<0. 001), the AKR1C3 level in the ventral prostate was significantly higher than that in the control group (P<0. 05, P<0. 01), AKR1C3 protein expression was increased, and a significant difference was found in the 270 μg/ kg group (P<0. 05). The AKR1C3 level in the dorsal prostate of the 30 and 90 μg/ kg groups was higher than that in the control group (P<0. 001, P<0. 05). Conclusions　Low-dose BPA and DEHP promotes AKR1C3 expression in the prostate of adult SD rats, but the sensitivities of ventral and dorsal prostate lobes to BPA and DEHP are different.

Abstract: Objective 　To explore the mechanism of baicalein inhibiting the proliferation and migration of laryngeal cancer cells. Methods 　Proliferation of Hep-2 laryngeal cancer cells was measured by MTT assays. Cell migration was assessed by a scratch assay. Apoptosis was detected by flow cytometry. Western blot was used to measure protein expression levels of Beclin-1, LC3II/ I, p62 and HDAC1. The expression level of miR-449a was measured by RTPCR. The binding sites of miR-449a and HDAC1 were analyzed by bioinformatics and identified by dual luciferase reporter assays. 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 Beclin-1 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 protein expression of HDAC1. Binding was observed between HDAC1 and miR-449a. Cotreatment of laryngeal cancer cells with Baicalein and an miR-449a mimic more significantly inhibited cell proliferation and HDAC1 protein expression, and more effectively upregulated miR-449a expression and induced autophagy. Conclusions　Baicalein mediated autophagy and inhibited the proliferation and migration of laryngeal cancer cells via the miR-449a/ HDAC1 axis.

Abstract: Objective 　To explore the effects of keratin 17 (Krt17) knockout on wound healing in diabetic mice. Methods 　To establish the diabetic model, a 60% high fat diet was provided and streptozotocin was administered intraperitoneally at 40 mg/ kg once per day for 5 consecutive days in wild type (WT) and Krt17 knockout (Krt17^{-/ -} ) mice at 6 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 1 week after successful modeling. Western blot and immunofluorescence staining were used to assess the expression and localization of KRT17, and histopathology of wound healing was analyzed on day 8. Images were taken at 0, 2, 4, 6, and 8 days after wounding, and the wound healing rate was calculated. Results　KRT17 was mainly expressed in mouse hair follicles under physiological conditions. When skin was injured, KRT17 expression in keratinocytes in the proximal wound was increased significantly. However, KRT17 expression in wounds of diabetic mice was significantly downregulated 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.

Abstract: Objective 　To investigate the effect of laminin subunit γ2(LAMC2) on the proliferation of gastric cancer cells through the PI3K/ Akt pathway. Methods 　Differentially expressed genes related to gastric cancer cell proliferation were analyzed in the cancer genome atlas and gene expression omnibus databases. The candidate gene LAMC2 was identified in accordance with the multiple of differential. UALCAN and Kaplan-Meier Plotter online databases were used to analyze LAMC2 expression in gastric cancer and its relationship with clinicopathological features. Western blot was used to detect LAMC2 in human gastric cancer cell lines HGC-27, NCI-N87 and SNU-1. An LAMC2 knockout gastric cancer cell model was established, and LAMC2 was detected by Western blot to determine the effects of model establishment. HGC-27 and NCI-N87 cells were divided into blank control(Control), negative control group(si-NC), and LAMC2 knockout(si-LAMC2)group. 5-Ethynyl-2’-deoxyuridine and colony formation assays were used to evaluate cell proliferation and clonality. Western blot was used to assess expression of cell proliferation-related proteins(Cyclin D1, PCNA and c-Myc)and activation of the PI3K/ Akt pathway. Results　LAMC2 was the most differentially expressed gene associated with cell proliferation in gastric cancer, and its expression was significantly upregulated in gastric cancer, which correlated to the clinicopathological characteristics of the gastric cancer stage, grade, and survival. The expression of LAMC2 in human gastric cancer cells (HGC-27, NCI-N87, SNU-1) was significantly higher than that in GES-1 cells(all P< 0. 01). Compared with the si-NC group, si-LAMC2 significantly inhibited HGC-27 and NCI-N87 cell proliferation, decreased the colony formation rate(P< 0. 01), and significantly decreased the expression of cell proliferation-related proteins(CyclinD1, PCNA and c-Myc) (all P< 0. 01). PI3Kp85 and Akt phosphorylation levels were also significantly downregulated( all P< 0. 01). Conclusions 　Upregulation of LAMC2 expression in gastric cancer is related to the clinicopathological characteristics of the gastric cancer stage, grade, and survival, and promotes cell proliferation by activation of the PI3K/ Akt pathway.

Abstract: 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/6J mice were randomly divided into control, DN and tubastatin A groups. Mice in DN and tubastatin A groups were intraperitoneally injected with 80 mg/ kg STZ daily for 3 days after removal of one kidney. The tubastatin A group received tubastatin A treatments every 3 days for 8 weeks. RNA-sequencing of differentially expressed genes was performed in kidney tissue of DN and tubastatin A groups. Mitochondrial damage was assessed by transmission electron microscopy. ROS levels in kidney tissue were estimated by DHE staining. Mouse glomerular endothelial cells (mGECs) were exposed to high glucose (HG) medium or 40 mmol/ L mannitol (control) with or without tubastatin A treatment. Western blot was used to analyze expression of HDAC6, kidney injury marker KIM1, and Epithelial-Mesenchymal Transition (EMT) markers. Flow cytometry was used to detect mitochondrial ROS and apoptosis in cells. Results　HDAC6 expression was upregulated in DN mouse kidney tissue and mGECs exposed to HG, which was consistent with the increased level 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 DMSO as the control, tubastatin A significantly decreased expression of KIM1, HDAC6, α-SMA, N-cadherin and vimentin (P<0. 05) and upregulated E-cadherin expression (P<0. 05) in mGECs under HG treatment. RNA-sequencing revealed enrichment of genes related to ECM-receptor interactions and the tricarboxylic acid cycle in kidney tissue of the Tubastatin A group compared with the findings in the DN group. Transmission electron microscopy showed that the proportion of damaged mitochondria in glomerular endothelial cells in the Tubastatin A group was significantly lower than that in the DN group (P<0. 01). The ROS level in kidney tissue of the Tubastatin A group was lower than that in the DN group (P< 0. 01). In mGECs, tubastatin A treatment downregulated HG-induced mitochondrial ROS levels (P<0. 01) and reduced apoptosis (P<0. 05). Conclusions　Tubastatin A ameliorates HG-induced glomerular endothelial cell injury and DN progression, and its mechanism is related to protection of mitochondrial homeostasis and inhibition of EMT.

Abstract: Objective 　Summarize the situation of laboratory animal licenses in China from 2018 to 2022, analyze the current situation and development trend of laboratory animal license management in China, and provide a basis for managing laboratory animals in China. Methods 　Laboratory animal license data were collated and preprocessed in accordance with the overall situation of the license, the four major regions licensed, the provinces (cities) licensed, the types of licensed animals, and different dimensions of the licensed environmental facilities. Data were analyzed and summarized through a combination of data statistics, graphical comparisons, related literature review, and comparative studies. Results　The overall trend of the number of laboratory animal licenses in China is increasing, fully reflecting the gradual realization of legalization and scientific supervision in the administrative license management of laboratory animals in China and the continuous improvement of the administrative license management efficiency and services. Conclusions This article describes and analyzes the developmental trend and existing problems of laboratory animal licenses in China and provides countermeasures and suggestions. It is recommended to improve the regulations and systems for laboratory animals, strengthen the supervision of administrative licenses for laboratory animals, and enhance the standardization of incremental resources for laboratory animals, which play an important role in promoting the development of China’s laboratory animal industry.

Abstract:Animal models are important means for basic research in traditional Chinese medicine (TCM). Qi deficiency, dampness, and blood stasis are the main syndromes of renal fibrosis. With the increase in the morbidity and mortality of chronic kidney disease, study of renal fibrosis animal models of qi deficiency and dampness stasis syndrome has become a hotspot in recent years. Additionally, establishment of combined disease and syndrome animal models is urgently needed. This article reviews the recent modeling method that established the renal fibrosis pathological model based on western medicine surgery and chemical factors, and established the model of qi deficiency, dampness and blood stasis disease from the aspect of etiology and pathology through the theory of exhaustion leading to qi loss or hunger leading to qi loss, internal and external dampness combination, exogenous pathogenic factors, and chemical drugs. Additionally, these studies established the evaluation standard of the renal fibrosis animal model of qi deficiency, dampness and blood stasis type from the aspects of macroscopic characterization, laboratory indexes, and pathological changes. The TCM disease and syndrome model has been combined with modern science to establish a relatively perfect qi deficiency and dampness stasis kidney fibrosis animal model with evaluation criteria. Exploring its pathogenesis and new treatments supports the therapeutic role of TCM in kidney fibrosis and promotes TCM internationally.

Abstract:Circular RNA (circRNA) is a type of non-coding RNA, in which 3’ and 5’ ends are joined together to form a covalently closed circular structure. Following ischemic stroke, the body undergoes various pathophysiological mechanisms, including oxidative stress, mitochondrial dysfunction, inflammation, endoplasmic reticulum stress, apoptosis, and autophagy. CircRNAs are involved in regulation of stroke by regulating the expression levels of ischemic stroke-related genes, mainly through sponge-adsorbed microRNAs. After ischemic stroke, some circRNAs have a protective effect on the brain, while others have a damaging effect on the brain. Studies suggest that circRNAs have the potential to provide new therapeutic approaches for ischemic stroke in the future. This article reviews the progress of circRNA research in the field of ischemic stroke and provides an outlook on the future applications of circRNAs.

Abstract:A high altitude plateau is a unique environment with low pressure, oxygen, and temperature. The plateau environment reduces the metabolism of energy substances and mitochondrial functions, thereby affecting work on a plateau. In recent years, mitochondrial damage has attracted broad attention. As the energy factory of cells, mitochondria are closely linked to body movement. 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 changes in important enzyme activities and the mitochondrial structure and function in the mitochondrial biochemical energy supply response. We 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, the tricarboxylic acid cycle, β-oxidation, and oxidative phosphorylation were inhibited, and the morphology and number of mitochondria were changed, leading to impaired mitochondrial functions and affecting exercise energy supply. Exploration of the mechanism of cell injury at high altitude may promote research to prevent and treat such injuries.

Abstract:Chronic obstructive pulmonary disease (COPD) is a common respiratory disease with high morbidity and mortality, and has become a major health issue. Traditional Chinese medicine has accumulated rich historical experience in the treatment of COPD and has unique clinical advantages. To further explore the therapeutic effect of traditional Chinese medicine on this disease, establishment of a COPD animal model combining disease and syndrome is critical to study occurrence and development of the disease. The combined models of disease and syndrome summarized 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-fluid syndrome. The common disease and syndrome in recent years combined with the method of class modeling are simply described and combined to provide new ideas for researchers and promote research of traditional Chinese medicine of this disease.

Abstract:Neurodegenerative diseases are chronic and progressive neurological diseases characterized by loss of a large number of specific neurons. They mainly include Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. Although the lesions and etiologies of various types of neurodegenerative diseases are different, delayed neurodegenerative lesions and cell loss in specific brain areas are common characteristics. For this reason, they are collectively referred to as neurodegenerative diseases. In recent years, zebrafish have attracted increasing attention as a new type of model organism. Although some differences exist 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 to study neurodegenerative diseases, and some achievements have been made in this field to improve our understanding of these diseases. However, because of the complexity, multiple factors, and multi-gene regulation of neurodegenerative diseases, the etiology and pathogenesis of zebrafish are unclear. Therefore, treatment of this kind of disease has been difficult. By consulting the relevant literature from home and abroad in recent years, this artcile reviews recent advances in neurodegenerative diseases using zebrafish as a model organism.

Abstract:Autophagy regulation of neurological diseases is the focus of current research in the field of neuroscience. Autophagy disorder leads to expression, deposition, and dysfunction of proteins such as Aβ, Tau, α-syn, and causes neurodegenerative diseases such as Alzheimer’ s disease, Parkinson’ s disease and Huntington’ s disease. Exercise is important to improve neurodegenerative diseases, which is closely related to upregulated expression of LC3, Beclin-1, Lamp1 and other autophagic factors after activation of AdipoR1/ AMPK/ TFEB, AMPK/ mTOR, and other pathways. A high autophagy level removes deposition of Aβ, Tau, α-syn and other proteins in the brain and improves neurodegeneration and synaptic structure and function disorder caused by neurodegenerative diseases. This article reviewed and analyzed the mechanism of autophagy in the improvement of neurodegenerative diseases by exercise, which provides a solid theoretical basis and new research ideas to improve neurodegenerative diseases by exercise.

Abstract:Exosomes are small molecule extracellular vesicles secreted by various cells and play a major role in the pathological process of Alzheimer’s disease by transporting various bioactive substances such as miRNAs. Expression of exosomal miRNA changes in the early stages of AD, and exogenous injection of mesenchymal stem cell-derived exosomal miRNA improves learning and memory of AD animal models. This article reviews the research progress of exosomes in early screening and treatment of Alzheimer’s disease.

Abstract: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 shown that gut microbiota regulates energy balance, glycolipid metabolism, and 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 prevention and treatment of metabolic diseases. In this article, we summarize the research progress of gut microbiota in the development and progression of obesity-associated metabolic diseases and analyze the role of gut microbiota in metabolic diseases.