Abstract: Objective To investigate the effect of Angelica polysaccharides on the balance of Th17 / T-regulatory( Treg) cells and the expression of related inflammatory factor proteins in the bone marrow of mice with aplastic anemia. Methods 50 male BALB / c mice were randomly divided into a normal group, model group, cyclosporine A(CsA) group,and angelica polysaccharide low-(APS-L) and high-dose(APS-H) groups. A mouse model of aplastic anemia was prepared by combining irradiation with allogeneic lymphocyte infusion. After modeling, the mice were orally administered with corresponding drugs for 28 days. The general condition, weight changes, and spleen index of the mice were observed.Blood samples were taken to test for changes in basic hematological parameters of peripheral blood, and hematoxylin and eosin staining was used to evaluate the pathological changes in mouse bone marrow tissue. An ELISA method was applied to detect bone marrow TGF-β1. The expression levels of proteins such as IL-10, IL-17A, and IL-6 were analyzed, and flow cytometry was used in detecting the bone marrow Th17 / Treg cell ratio. Results Compared with the normal group, the model group mice showed clumsiness during activity; lethargy; pale eyelids, lips, and ears; and reduced food and water intake. Both body weight and spleen index were significantly decreased. Peripheral red blood cell, white blood cell, and platelet counts and hemoglobin concentration were significantly reduced. A disordered bone marrow tissue structure and significantly reduced proliferation of hematopoietic tissue were seen. The expression of IL-17A and IL-6 proteins was significantly upregulated, and the expression of TGF-β1 and IL-10 protein was significantly downregulated. The proportion of Th17 cells in bone marrow significantly increased, the proportion of Treg cells significantly decreased, and the ratio of Th17 / Treg cells significantly increased (P<0. 01) . Compared with the model group, the general condition of the APS-L and APS-H groups improved, showing an increase in food and water intake; a significant increase in body weight and spleen index; a significant increase in peripheral red blood cells, white blood cells, platelets, and hemoglobin concentration ( P<0. 05 ) ; an improvement in bone marrow tissue structure; and an increase in hematopoietic tissue proliferation (P<0. 05) . The expression of IL-17A and IL-6 proteins was significantly downregulated. The expression of TGF-β1 and IL-10 protein was significantly upregulated ( P<0. 05 or P<0. 01) . The proportion of Th17 cells in bone marrow significantly decreased, the proportion of Treg cells significantly increased, and the ratio of Th17 / Treg cells significantly decreased ( P<0. 01 ) . Conclusions Angelica polysaccharides can improve bone marrow hematopoietic function in aplastic anemia mice, and its mechanism of action may include the regulation of Th17 / Treg cell balance.

Abstract: Objective To observe the effects of folic acid ( FA) supplementation on the expression of Flotillin-1 and β-amyloid protein ( Aβ) -metabolism-related proteins in the brains of inflammation-stimulated Alzheimer’ s disease (AD) mice. Methods Twenty-seven 6-month-old male APP / PS1 mice were randomly divided into AD, AD+LPS, and AD+LPS+FA groups, with nine mice in each group. Nine C57BL / 6J male mice born within the same month were used as the Control group. The AD + LPS + FA group was given folic-acid-supplemented feed ( 8 mg / kg ) for 3 months of intervention, while the other three groups were fed normal feed. Lipopolysaccharide solution ( LPS, 250 μg / ( kg·d) ) was injected intraperitoneally into mice in the AD+LPS and AD+LPS+FA groups 1 week before the end of the experiment, and saline was injected into the remaining two groups. The serum inflammatory factors TNF-α and IL-6 levels and brain tissue Aβ1- 40 and Aβ1- 42 levels of mice in each group were detected by ELISA. Flotillin-1 protein expression in brain tissue was detected using Western blot, and the co-expression of Flotillin-1 and Aβ1- 42 / APP / PS1 / BACE1 in the cortical region of the brain was detected via immunofluorescence double-labeling. Results After ANOVA analysis, we found mice in the AD group had elevated serum TNF-α and IL-6 levels ( P<0. 05) , elevated levels of Aβ1- 40 and Aβ1- 42 ( P<0. 05) , increased expression of Flotillin-1 protein (P<0. 05) , and increased co-expression of Flotillin-1 and Aβ1- 42 / APP / PS1 / BACE1 in the cortical brain tissue (P<0. 05) compared with the Control group. Compared with mice in the AD group, those in the AD+LPS group had further increases in serum inflammatory factors and Aβ levels in the brain ( P<0. 05) and increased coexpression of Flotillin-1 and Aβ1- 42/ APP / BACE1 double-labeled proteins in their cortical brain tissue ( P<0. 05 ) .Compared with mice in the AD+LPS group, those in the AD+LPS+FA group had lower in vivo inflammation levels and Aβcontent in the brain ( P<0. 05) , lower brain tissue Flotillin-1 protein expression ( P<0. 05) , and lower Flotillin-1 and Aβ1- 42 / APP / PS1 / BACE1 protein co-expression in cortical brain tissue ( P<0. 05 ) . Conclusions Folic acid supplementation may reduce Flotillin-1 protein expression and Aβ deposition in the brain of AD inflammatory mice.

Abstract: Objective To assess the feasibility of establishing a nude mouse model of endometriosis fibrosis of human origin and to determine whether endometrial mesenchymal stem cells are involved in inducing endometriosis fibrosis. Methods Four endometrial tissue specimens were collected and transplanted 1 ∶ 3 into 12 BABL / c nude mice by subcutaneous injection. The morphology and volume of the lesions were recorded. The nude mice were sacrificed on the 15th day after transplantation to observe the morphology of the lesions and their adhesion to the periphery of the abdominal wall. HE staining was used to judge the result of modelling, Masson staining was used to assess the extent of fibrosis, and immunofluorescence was used to track the role of endometrial mesenchymal stem cells in the fibrotic process of endometriosis. Results The volume of ectopic lesions in nude mice increased over time and showed restricted, vesicularlike changes. The tight adhesion of the lesions to the abdominal wall, endometrioid glands, and collagen fiber deposition were seen microscopically. The success rate of the modelling was 83. 4%, and the collagen fiber volume fraction of the lesions was significantly higher after modelling (P<0. 01) . Confocal imaging suggested that endometrial mesenchymal stem cells ( SUSD2⁺) differentiated into myofibroblasts (α-SMA⁺) in vivo. Conclusions The nude mouse model established by human allogeneic transplantation via subcutaneous injection was consistent with the lesion characteristics of endometriosis fibrosis. The modelling method is simple and feasible and provides a better reference model for further investigating the pathogenesis of endometriosis fibrosis. In addition, in vivo observations using the model indicated that endometrial mesenchymal stem cells are involved in inducing the formation of endometriosis fibrosis.

Abstract: Objective To analyze the morphological and structural changes to pulmonary arterioles in rats induced by smoke exposure combined with Klebsiella infection, and to evaluate the severity of the pulmonary arteriolar lesions. Methods Pulmonary arteriolar images from lung sections of control and model rats treated with smoke exposure combined with Klebsiella infection were analyzed by qualitative and quantitative method. Victorian-blue-stained sections were used for the detection of pulmonary arteriolar muscularization, vascular wall thickness, vascular occlusion score, the intima thickness and media thickness of muscular arterioles, and neointima proliferation. Hematoxylin and eosin-stained sections were used for the observation and detection of inflammatory cell infiltration and plexiform lesions around arterioles. Van Gieson-stained sections were used for the observation of collagen fibers in the intima and detection of the percentage of collagen fiber area in the arteriolar wall. Based on the above analyses, the degree of pulmonary arteriolar pathology was rated according to Heath-Edwards criteria. Results For ≤ 50 μm diameter arterioles, the percentage of non-muscular vessels was significantly decreased(P<0. 01) , the percentage of muscular vessels was increased(P<0. 01) , the percentage of partial muscular vessels was not significantly different(P>0. 05) , the thicknesses of the non-muscular vessel walls and muscular vessel walls were significantly increased(P<0. 05,P<0. 01) , and the occlusion scores of both non-muscular and muscular pulmonary arterioles were significantly increased in the model group compared with the Control group(P<0. 05,P<0. 01) . For 50 μmP<0. 05) , the percentages of muscular vessels and partial muscular vessels were not significantly different(P>0. 05) , the wall thickness and occlusion score of muscular vessels were significantly increased ( P<0. 05 ) , and the wall thickness and occlusion score of non-muscular vessels were not significantly different in the model group compared with the Control group (P>0. 05) . Compared with the Control group, the model group showed significantly increased intimal thickness and media thickness and significantly increased perivascular inflammatory infiltration score in both muscular arterioles of ≤ 50 μm diameter and 50 μmP<0. 05,P<0. 01) . In the Control group ( n= 9) , only one section with two neointimal lesions was found, and the degree of neointima proliferation was 1. 61%. In the model group ( n= 10) , five sections had neointima lesions, and the degree of neointima proliferation was 1. 04% to 17. 14%. No plexiform lesions were found in any section. For pulmonary arterioles with a diameter of ≤100 μm, there was no change in the expression of intimal collagen fibers in the model group compared with the Control group, and there was no significant difference in the percentage of collagen fiber area in the vessel walls ( P>0. 05) . According to Heath-Edwards criteria, the pulmonary arteriole lesions in the model rats did not reach grade III. Conclusions The model rats showed pathological manifestations such as pulmonary arteriolar muscularization, thickening of the intima and media, and mild to moderate inflammatory reactions around arterioles. The low amount of neointimal proliferation and collagen fibers in the vascular wall and the absence of plexiform lesions suggest that the model may be up to grade II lesions, according to the Heath-Edwards criteria.

Abstract: Objective Bibliometric approaches are used to investigate the characteristics and benefits of traditional Chinese medicine treatments for dominant diseases that can be applied in clinical therapy to effectively manage geriatric diseases. Methods Clinical research literature on the use of traditional Chinese medicine in the treatment of geriatric diseases within the past 10 years was retrieved from CNKI, Wanfang, VIP, and CBM databases. The research trends and clinical efficiency of each disease were statistically analyzed to determine the dominant diseases of TCM. Results A total of 22 859 articles were collected, with 3768 included in the research. In accordance with the International Statistical Classification of Diseases and Related Health Problems ( ICD-11) of the World Health Organization, the diseases were classified into 17 categories and 149 diseases. The diseases primarily affect the circulatory system, skeletal musculoskeletal or connective tissue system, and digestive system. Conclusions Traditional Chinese medicine clinical trials on the treatment of geriatric illnesses cover a diverse spectrum of diseases, although the distribution of focus is unequal. Potential dominant illnesses were eventually identified to include osteoporosis, constipation, and hypertension,with heart failure, stroke, coronary heart disease, diabetes and its complications, and insomnia being potential subdominant diseases.

Abstract: Objective To establish a rat model of hyperuricemic nephropathy ( HN) using a multifactorial induction method of potassium oxazinate combined with adenine and yeast feed to observe the intervention effect of Qiling granules (QLG) . Methods Fifty-eight SPF-grade male SD rats were selected, and 10 rats were randomly allocated to the normal control (NC) group. The remaining rats were induced by multiple factors to establish HN rat models. After 2 weeks of modeling, submandibular blood samples were taken to detect serum UA, CREA, BUN, TG, and TC. Forty HN rats with bleeding clearance UA and body weight close to the mean were selected. They were randomly divided into a model ( M) group, QLG low dose (QLG-L) groups, QLG high dose (QLG-H) group, and a positive control ( PC) group, with 10 rats in each group, using a stratified randomization method. Each group was given corresponding drugs by gavage daily, and after continuous administration for 4 weeks, submandibular blood samples were taken to detect serum UA, CREA, BUN, TG, and TC. After euthanasia of the rats, liver tissue was taken to detect XOD and ADA activity. Renal tissue was taken for HE and Gomori hexamine silver staining, and the protein expression of GLUT9, OAT1, VCAM-1, and TGF-β in the kidneys was observed using immunohistochemistry and Western blot method. Results Compared with the NC group, the M group’ s serum levels of UA, CREA, BUN, TC, and TG, as well as liver XOD and ADA activities, were significantly increased (P<0. 01) . The renal tissue of the model rats showed significant pathological changes. The area of renal tubules positive for urate and the expression of GLUT9, VCAM-1, and TGF-β proteins in the kidneys were significantly increased (P<0. 01, P<0. 05) ,while the expression of OAT1 was significantly reduced ( P<0. 01) . Compared with the M group, each treatment group showed significantly reduced serum UA levels, liver XOD, ADA activity, and renal VCAM-1 protein expression (P<0. 01, P<0. 05) . The serum CREA and BUN levels and renal TGF-β protein expression of rats in the QLGL group were significantly reduced ( P<0. 05, P<0. 01) . The serum CREA and BUN levels and renal GLUT9 protein expression of rats in the QLG-H group were also significantly reduced (P<0. 01, P<0. 05) . The urate deposition and renal injury caused by each treatment were reduced to varying degrees, but there were no significant differences among groups (P>0. 05 ) . Conclusions A stable HN rat model can be induced by gavage of potassium oxyzinate and adenine in combination with yeast feed. QLG can effectively treat HN by improving UA metabolic disorders, reducing the renal inflammation and urate deposition that cause renal damage in HN model rats. Its mechanism of action is related to a reduction in serum UA, CREA, BUN, and TG levels; liver XOD and ADA activities; and the expression of GLUT9,OAT1, VCAM-1, and TGF-β proteins in the kidneys.

Abstract: Objective To investigate the effects of ethanol extract of Akebia trifoliate ( Thunb. ) Koidz (EEATK) on the proliferation and apoptosis of human hepatocellular carcinoma Hep3B and Huh-7 cells and to explore its underlying mechanism. Methods Human Hep3B cells and Huh-7 cells were cultured in vitro and separated into control group,Sorafenib group (5 μmol / L) , and EEATK groups ( 0. 10 mg / mL, 0. 15 mg / mL, 0. 20 mg / mL, 0. 3 mg / mL) and given the corresponding drug interventions. A CCK-8 assay was used to measure the impact of the different interventions on the proliferation of Hep3B cells and Huh-7 cells to screen the optimal action-inducing concentrations for subsequent experiments. EdU staining assay and colony formation assay were used to explore the effect of EEATK on proliferation, and Annexin V-FITC / PI double-staining assay was applied for apoptotic rate analysis. Transcriptome sequencing ( RNA-seq) technology was used to analyze differentially expressed genes ( DEGs) related to cell proliferation and apoptosis in the control group and EEATK ( 0. 15 mg / mL) groups of Hep3B cells. DEGs were analyzed for function with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes ( KEGG) pathway enrichment. The Comparative Toxicogenomics Database(CTD) was used to validate the expression of key proteins related to cell proliferation and apoptosis, and the findings were verified by qRT-PCR. Results Compared with the control group, different concentration of EEATK significantly inhibited the activity of Hep3B and Huh-7 cells ( P<0. 01) . Hep3B cells were treated with 0. 15 mg / mL EEATK, the EdU-positive cell rate and clone formation rate significantly decreased ( all P<0. 01) . At the same time, the apoptotic rate of the EEATK group significantly increased ( P<0. 01) . Transcriptome sequencing of Hep3B cells showed that EEATK induced significant changes in the expression of 1577 genes (P<0. 01) , of which 942 were up-regulated and 635 were down-regulated compared with the control group. GO functional enrichment analysis revealed that the DEGs were mainly enriched for cholesterol synthesis, inflammation, and extracellular matrix. KEGG pathway analysis showed that EEATK plays an anti-tumor role, mainly through the TFG-β and NF-κB signaling pathways. CTD and qRT-PCR analysis showed that EEATK significantly down-regulated the expression of apoptosis-related genes such as BIRC5 and CDK1 ( P<0. 01) and significantly upregulated the expression of CDKN1A and EGLN3 (P<0. 01) . At the same time, EEATK caused the significant downregulation of cell-proliferation-related genes such as FAM83D and MKI-67 (P<0. 01) , and significantly upregulated the expression of MYC and FOXC1 ( P<0. 01 ) . Conclusions EEATK can inhibit cell proliferation and induce apoptosis in a manner that may be related to the regulation of TGF-β and NF-κB signal pathway-related gene expression.

Abstract: Objective To detect the apoptosis effects of dioscin in HepG2 cells and its possible antihepatocellular carcinoma mechanisms. Methods HepG2 human hepatocellular carcinoma cells were exposed to 0. 25,0. 5, 1, 2, 4, 6, or 8 μmol / L dioscin, and cell proliferation was measured via MTT assay. The half-maximal inhibitory concentration ( IC50) was calculated with the software. A scratch test was used to analyze cell migration ability. Western blot was employed to evaluate the expression of apoptosis and Wnt / β-catenin-pathway-related proteins. Results Compared with the control group, the dioscin-treated HepG2 cells’ proliferation was significantly more inhibited, and the inhibition increased in a time- and dose-dependent manner (P<0. 01) . HepG2 cells showed morphological characteristics of apoptosis after they were treated with 1 μmol / L or 2 μmol / L dioscin. The scratch test indicated that the migration distance of HepG2 cells was remarkably reduced when treated with dioscin. In the Western blot experiment, the expression levels of Caspase3 and cleaved Caspase-3 were visibility up-regulated, while those of Bcl-2 and β-catenin were significantly down-regulated when the cells were treated with dioscin for 24 h (P<0. 05, P<0. 01) . When LiCl reagent was added to the HepG cells to activate the Wnt / β-catenin signaling pathway, the expression levels of Wnt1 and β-catenin were remarkably increased compared with those of the control group (P<0. 01) . Compared with the LiCl group, the LiCl + DIO group’ s expression of Wnt1, β-catenin, and GSK-3β was significantly decreased ( P<0. 01) . Conclusions DIO can promote the apoptosis of HepG2 cells by inhibiting β-catenin protein expression and thereby down-regulating the Wnt / β-catenin signaling pathway. This inhibits apoptosis-related gene Bcl-2 expression, which leads to the induction of cell apoptosis. Therefore, DIO can have an anti-hepatocellular carcinoma effect.

Abstract: Objective To observe whether the IL-23 / Th17 inflammatory pathway is involved in the development of calcific aortic valve disease, and whether secukinumab can delay the progression of calcific aortic valve disease by inhibiting this pathway. Methods Forty-seven mice were divided into a blank control group, model group, and secukinumab group according to the random number table method. The blank control group was fed normal chow, while the model group and secukinumab group were fed pro-calcification chow for 16 weeks to establish a calcific aortic valve disease model. After intervention with secukinumab for 4 weeks, peak flow velocity changes in the aortic valves were detected under Doppler ultrasonography in all mice. Relevant indexes were determined by hematoxylin and eosin staining, Von Kossa staining, immunohistochemical staining, ELISA, and qPCR. Results Compared with the model group, the secukinumab group showed significantly reduced peak flow velocity ( P<0. 05) and serum IL-6, IL-17, and IL-23 levels (P<0. 05 ) in the aortic valve. Compared with the secukinumab group, the model group ’ s leaflet thickness was significantly increased, and there were more calcium deposits. Immunohistochemical result showed that macrophage infiltration ( P<0. 05 ) , IL-17A ( P<0. 05 ) and IL-23 ( P>0. 05 ) levels in the valve leaflets were reduced in the secukinumab group compared with the model group. PCR result suggested that the expression of STAT3, BMP-2, and αSMA mRNA was significantly lower in the secukinumab group than the model group (P<0. 05) . Conclusions The IL-23 /Th17 inflammatory pathway is involved in the pathogenesis of calcific aortic valve disease. The inflammation, fibrosis,osteogenic differentiation, and calcification of mouse valves were alleviated after intervention with secukinumab, which may delay disease progression by inhibiting the IL-23 / Th17 inflammatory pathway.

Abstract: Objective A sterile golden hamster model was established by cesarean section purification. Methods SPF-grade donor female golden hamsters were selected, and males and females were mated 1 ∶ 1 and separated after mating. The cage time of the surrogate mothers was 1 week earlier than that of the donor mothers. Parturient golden hamsters underwent hysterectomy on a sterilized workbench, and the uteruses were transferred into isolation kits and stripped. To obtain sterile milk for milk replacement, sterile ICR mice and sterile SD rats were used. After successful separation, the hamsters were transferred to isolation kits to prepare for feeding. The sterility status of the feeding isolation kits was tested monthly. Results Three caesarean sections were performed, but the first and second lactations failed. The third milk replacement was successful, and 18 young hamsters were obtained with survival rates of 88% and 66% after weaning. All hamsters were quality tested by GB / T 14926. 41-2001. Conclusions Using a cesarean section purification technique and sterile ICR mice and SD rats for microbial-free milk replacement, a sterile golden hamster model was obtained.

Abstract:Graduate students are the main practitioners of animal experiments in universities. However, a lack of professional skills and management standards for education on laboratory animals in medical graduate student courses has led to frequent violations of animal experimental guidelines and poses a significant biosafety risks. To ensure the quality of animal experiments and improve the research quality and skills of graduate students, with reference to current practices, this article proposes an innovative teaching model combining a Laboratory Animal Science course with training for medical graduate students. We suggest reforms to teaching content according to scientific research needs, recommend improvements in teaching method, and analyze the significance of the teaching-training model. Our review was written to propose new ideas for strengthening graduate students ’ awareness of animal experiment standardization and improve their scientific research literacy, as well as provide a reference for animal experiment standardization for educators of domestic medical students.

Abstract:Ferroptosis is a non-apoptotic mode of cell death characterized by iron-dependent lipid-peroxideaccumulation-induced membrane lipid peroxidation and mitochondrial atrophy. It differs from other programmed cell deaths in its morphological and biochemical properties. Ferroptosis is regulated by a variety of metabolic pathways that are involved in the acute lung injury induced by hemorrhagic shock, ischemia-reperfusion, sepsis, and radiation. This article reviews the main regulatory mechanisms of ferroptosis and its role in the pathogenesis of acute lung injury in various animal models with the aim of providing new strategies for the prevention and treatment of acute lung injury.

Abstract:Depression is a psychosomatic disorder. The rising incidence rate of depression in recent years is placing a heavy economic burden on societies around the world. Morinda officinalis oligosaccharides ( MOOs) are active substances extracted from the Chinese herb Morinda officinalis that can soothe depression and calm the mind, tonify the kidneys, and benefit the intellect, as well as improve cognitive disorders in patients to a certain extent. On the basis of the hypothesised pathological mechanism of depression, this study explains the link between MOOs and depression by reviewing existing studies. We propose that MOOs can improve depression through mechanisms that regulate the levels of monoamine neurotransmitters, enhance neuroplasticity, regulate the function of the HPA axis and levels of cytokines, and influence gut microbiota. This paper provides new ideas for research on the antidepressant effects of MOOs.

Abstract:On the basis of the clinical characteristics of atherosclerosis ( AS) in traditional Chinese medicine ( TCM) and Western medicine, this paper analyzes common animal models of AS. The coincidence of clinical characteristics of the models was scored in the hope of providing new ideas and a reference for those studying AS.This paper reviews the varieties, modeling method, modeling principles, and characteristics of common animal models of AS. Moreover, similarities among common animal models, in terms of their clinical diagnostic criteria and symptom characteristics, were assessed. High-fat feeding type, mechanical injury combined with high-fat feeding type, genetic engineering combined with high-fat feeding type, chemical induction combined with high-fat feeding type, and combined Chinese clinical syndrome and Western disease AS models are widely established. Comparative analysis showed that balloon injury combined with high fat feeding type, ApoE receptor-knockout mouse combined with high-fat diet type, and phlegm and blood stasis type models of disease and symptom combinations showed a comparatively high level of clinical agreement between Chinese and Western medicine. Presently, most animal models of AS have a high degree of relevance to Western medicine, and the evaluation criteria used for the models are predominately from a Western medicine perspective. Models that combine disease and syndrome are lacking, hindering the development of wholism concepts and treatment through the differentiation of syndromes used in TCM. Therefore, establishing an animal model with a high degree of accuracy and coincidence between TCM and Western perspectives that combines the disease and its TCM symptoms is a top priority for studying the prevention and treatment of AS.

Abstract:Ankylosing spondylitis is an autoimmune disease with sacroiliac arthritis and spinal arthritis as the main manifestations. The disease mainly occurs in young men, has a high disability rate, and is a serious threat to the life and health of patients. Biological agents are expensive, and many adverse reactions to hormones, non-steroidal antiinflammatory drugs, and anti-rheumatic drugs have been recorded. Traditional Chinese medicine can regulate the immunity and anti-inflammatory effects of the disease, and has good clinical effects. To promote the further study of the pathogenesis of ankylosing spondylitis and the development and screening of therapeutic drugs and therapies, in this paper, we summarize the method and mechanisms of modeling of the existing animal model of ankylosing spondylitis and analyze the advantages and disadvantages of the model. To evaluate the agreements between Chinese and Western medicine clinical characteristics, we compare the characteristics of Chinese and Western medical syndromes of the animal model. Building an animal model of ankylosing spondylitis with a higher degree of consistency between traditional Chinese and Western medicine is the key to innovative research into traditional Chinese medicine method of treating ankylosing spondylitis. To lay the foundation for research into traditional Chinese medicines and acupuncture for ankylosing spondylitis, this paper analyzes the degree of concurrence between the Chinese and Western medicine clinical characteristics of animal models.

Abstract:The Nod-like receptor pyrin domain-associated protein 3 ( NLRP3) -mediated pyroptosis of pulmonary parenchymal and immune cells plays a key role in the pathogenesis of lung injury during sepsis. NF-κB, JAK2 / STAT3 and MAPK signaling pathways are involved in NLRP3-mediated pyroptosis. Targeting NLRP3-pyroptosis and its related signaling pathways, pharmacological interventions with Physalin B, schisandrin, erythropoietin, and physical therapies such as acupuncture at Zusanli and Feishu points, as well as NLRP3-specific inhibitors like ergolide, have all shown effective anti-septic effects in treating lung injuries. This article reviewed the roles and mechanisms of NLRP3-pyroptosis in sepsis-induced lung injury, as well as the experimental progresses made in targeting NLRP3 pyroptosis as a therapy. We aim to highlight the importance of NLRP3-pyroptosis as a target, providing insights for the prevention and treatment of sepsis-induced lung injury.

Abstract:Inflammatory skin diseases ( ISD) are characterized by persistent inflammatory cell infiltration and lingering and intractable skin lesions. At present, corticosteroids are the main drugs used in the treatment of ISD.However, due to the characteristics of recurrent and intractable ISD, long-term use of these hormone drugs may cause serious side effects in patients. In recent years, increasingly more studies are confirming that bee venom has significant anti-inflammatory, anti-apoptosis, anti-fibrosis, antibacterial, and other effects and could effectively treat ISD. In this paper, the main active components and anti-inflammatory mechanisms of bee venom are reviewed. The latest attempts to use bee venom for acne, atopic dermatitis, psoriasis, urticaria, and systemic lupus erythematosus are discussed, providing a reference for basic research and the clinical treatment of ISD.

Abstract:In recent years, psoriatic arthritis has become a major problem in the medical field, with cases gradually increasing in China, and it is still incurable. Here, we summarize the pathogenesis and clinical characteristics of currently available animal models of psoriatic arthritis based on Chinese and Western medical evidence. Literature in line with this topic was collated and summarized. The etiology and pathogenesis according to Chinese and Western medicine of existing psoriatic arthritis models were given agreement scores; the diagnostic criteria of Chinese and Western medicine were compared; and the models’ characteristics and degree of agreement with clinical observations were assessed. This study found that the human leukocyte antigen transgenic mouse model, the multiple hybridization transgenic mouse model,and the mannan-induced mouse model had the highest agreement scores. As psoriatic arthritis is more common in Europe, Methods for the preparation of animal models have been mostly imported from abroad, and very few animal models have the characteristics of Chinese medicine; therefore, the model fitness scores of Western diagnoses were higher than those of Chinese diagnoses as a whole. We hope to leverage the unique diagnosis and treatment method of Chinese medicine further to improve the types of psoriatic arthritis animal models available. This study provides a basis for the construction of improved animal models of psoriatic arthritis with combined traditional Chinese and Western medicine characteristics.

Abstract:Depression, a common mood disorder, has a complex pathogenesis. In recent years, the accelerated pace of life has been accompanied by an increase in the prevalence rate of depression, leading to extensive attention being given to this condition. External stress and inflammation synergize to damage blood vessel and brain functions, induce immune disorders, cause microglia activation, and increase the expression of pro-inflammatory cytokines and their receptors. Inflammatory reactions continue to escalate, which affects the normal metabolism and metabolism of the neurotransmitter system. The abnormal functioning of molecular pathways leads to mutations in brain cell and nerve genes, and further formation of the immune-inflammation-neuron cycle pathway becomes an important mechanism in the occurrence and development of depression. A large number of studies have shown that traditional Chinese medicines can improve depression symptoms by restoring neuroimmune inflammation homeostasis. This article explains neuroimmune inflammation’ s close connection with depression and its pathogenesis and reviews the role of various traditional Chinese medical therapies in improving and treating depression by participating in the regulation of neuroimmune inflammation. This review provides new perspectives on the precise treatment of depression and the development of immune-targeted drugs.