Abstract: Objective To observe the protective effect of atorvastatin on joint injury in ApoE^{- / -} mice. Methods Forty ApoE^{- / -} mice were randomly divided into a model group and a drug group. All mice were fed a high-fat diet. The drug group received atorvastatin 10 mg / (kg·d), and the model group received the same amount of normal saline. Twenty normal C57BL/ 6J mice (control group) were fed a normal diet. We used an automatic biochemical analyzer to detect changes in blood lipids, and ELISA was used to detect serum IL-6 and TNF-α concentrations. Knee joint tissue samples were harvested for HE staining and safranin O-fast green staining to observe tissue morphological changes, and transmission electron microscopy was used to observe chondral ultrastructural changes. Results Compared with the model group, serum TC, TG, and LDL-C concentrations in the atorvastatin ( drug) group were significantly decreased (P<0. 01), while HDL-C concentrations increased (P<0. 01), and the serum inflammatory factors, IL-6 And TNF-α decreased significantly (P< 0. 01). Chondral ultrastructural damage improved significantly with atorvastatin. Inflammatory cell infiltration in the synovial membrane of the knee joint decreased, as did the degree of cartilage tissue structural damage and ossification, which significantly delayed the disease process. Conclusions Atorvastatin can protect against joint damage in ApoE^{- / -} mice by regulating blood lipids and down-regulating inflammatory factors.

Abstract: Objective To explore the mechanism of phosphoramide mustard (PM)-induced ovarian granulosa cell damage and the effect of serum containing Zuogui pill on autophagy and apoptosis of damaged granulosa cells. Methods Serum containing Zuogui pill was prepared and primary rat ovarian granulosa cells were cultured in vitro. At 75% ~ 80% confluence, the cells were divided into four groups: group 1: control; group 2: model (M); group 3: serum containing Zuogui pill ( 10% ZGW); and group 4: model + serum containing Zuogui pill ( M + 10% ZGW). The model of chemotherapy-induced granulosa cell injury was established in groups 2 and 4 after PM treatment for 24 hours. In groups 1 and 2, 10% normal rat serum was added. In groups 3 and 4, 10% serum containing Zuogui pill was added, followed by culture for 24 hours at 37℃ with 5% CO₂ . Flow cytometry was used to detect the apoptosis rate of granulosa cells in each group and expression of Beclin-1, LC3B, P62, Bax, and Caspase-3 was detected by Western blot. Results Compared with the control group, the apoptosis rate of the model group was increased significantly, expression of Beclin-1, LC3B, Bax, and Caspase-3 protein was increased, and expression of P62 protein was decreased (P< 0. 05). The 10% serum containing Zuogui pill significantly reduced the apoptosis rate of granulosa cells in the model group, downregulated the expression of Beclin-1, LC3B, Bax, and Caspase-3 protein in damaged granulosa cells, and upregulated the expression of P62 protein in damaged granulosa cells ( P< 0. 05). Conclusions PM damages ovarian granulosa cells, promotes apoptosis of granulosa cells, and activates the autophagy / lysosome degradation pathway in granulosa cells. The 10% serum containing Zuogui pill reduces the apoptosis rate of chemotherapy-treated granulosa cells, which is related to expression of autophagy proteins.

Abstract: Objective To investigate the induction of abdominal aortic aneurysm by DOCA plus high salt at different time points and the undeR_Lying molecular mechanism. Methods Ten-month-old C57BL/ 6J mice were divided into two groups: a high-salt group (HS) and a DOCA plus high-salt group (DOCA+HS). Each group received the designated treatments for 1 week, 2 weeks, and 3 weeks. At the end of treatment, the mice were anesthetized with isoflurane followed by ultrasonography and aorta collection to observe abdominal aorta expansion and aneurysm formation. H&E staining, Masson’ s staining, and elastic fiber staining were performed to detect pathological changes, collagen deposition, and elastic fiber fragmentation, respectively. Immunohistochemistry was used to detect abdominal aortic inflammatory cell infiltration, and RT-PCR was used to detect the mRNA expression of inflammatory and anti-inflammatory factors. RNA sequencing was conducted to analyze the differentially-expressed genes and the enrichment signaling pathways of these genes in the arterial tissues of the two groups of mice after 3 weeks of treatment. Results Compared with the HS group, DOCA+ HS treatment for 1 week did not induce the formation of abdominal aortic aneurysms in mice, but after 2 weeks of treatment, the mice began to form aortic aneurysms. The incidence of aortic aneurysm was 44% at week 2 and 65% at week 3. With increased duration of DOCA+HS treatment, collagen deposition in the abdominal aorta increased, and elastic fiber fragmentation was observed. Meanwhile, high inflammatory cell infiltration (mainly macrophages and T cells) was observed in the abdominal aorta of mice after treatment with DOCA+HS for 2 weeks and 3 weeks. The mRNA levels of inflammatory factors increased significantly, while the mRNA levels of anti-inflammatory factors decreased. Additional transcriptome sequencing result showed that the differentially-expressed genes in the two groups of mice after 3 weeks of treatment were enriched mainly in the immune system and metabolic pathways, and that levels of the key molecule PSGL-1, which mediates leukocyte adhesion, increased significantly after 3 weeks of DOCA+ HS treatment. Conclusions DOCA+ HS treatment can induce abdominal aortic aneurysm formation in mice after 2 weeks of therapy. PSGL-1 and its mediated inflammation may play important roles.

Abstract: Objective To investigate the effect and mechanism of valsartan on high glucose-induced rat kidney cell proliferation and apoptosis. Methods High glucose was used to induce HBZY-1 damage in rat mesangial cells, and different concentrations of valsartan were given. Western blot detected of proliferation and apoptosis-related proteins CyclinD1, Cleaved caspase-3, Bcl-2 related X protein ( Bax), B cell lymphoma / leukemia - 2 ( Bcl-2), and NOTCH1 signaling pathway protein jagged1, NOTCH1 expression, MTT colorimetric method was performed to determine cell proliferation activity, and flow cytometry was applied to evaluate cell cycle and apoptosis. The high glucose-induced HBZY- 1 was treated with NOTCH1 signaling pathway activators Jagged 1 / Fc fusion protein and valsartan, and its effects on cell proliferation, cell cycle and apoptosis were observed. Results The expression level of CyclinD1, Bcl-2 protein, cell proliferation activity at 24 h, 48 h and 72 h, and S-phase cell ratio in HBZY-1 induced by high glucose were significantly decreased, and G0-G1-phase cell ratio, Cleaved caspase-3, Bax, jagged1 and NOTCH1 protein expression levels and apoptosis rate were greatly increased (P<0. 05). 0. 01, 0. 1, 1 μmol / L valsartan obviously improved the expression levels of CyclinD1, Bcl-2, cell proliferation activity at 24 h, 48 h and 72 h, and S-phase cell ratio, while dramatically reduced G0-G1-phase cell ratio, the expression levels of Cleaved caspase-3, Bax, jagged1, NOTCH1 and the apoptosis rate, all in a concentration-dependent manner (P<0. 05). NOTCH1 signaling pathway activator Jagged 1 / Fc fusion protein partially reversed the effects of valsartan on the proliferation, cell cycle and apoptosis of HBZY-1 treated with high glucose. Conclusions Valsartan can promote the proliferation and cell cycle of rat mesangial cells treated with high glucose by inhibiting the NOTCH1 signaling pathway, and reduce the apoptosis.

Abstract: Objective To study the inhibitory effects of Fuzheng Kang-Ai (FZKA) decoction on the migration and invasion of human ovarian carcinoma (HO-8910PM) cells and the undeR_Lying mechanisms. Methods Forty-eight SD rats were randomly divided into a control group, low-dose FZKA group (4. 725 g / (kg·d)), medium-dose FZKA group (9. 45 g / (kg·d)), and high-dose FZKA group (18. 9 g / (kg·d)). The drug was administered by gavage once per day for 7 days. The decoction was isolated and used to incubate HO-8910PM cells, and changes in the related indices were detected by the cell scratch test, transwell assay, ELISA, real-time quantitative PCR, and Western blot. Results Compared with the control group, after 24 hours of low -, medium-, and high-dose FZKA decoction treatment, HO-8910PM cell mobility and invasion were significantly lower ( P< 0. 01). Compared with the control group, after 12 -, 24 -, and 48 h of low -, medium-, and high-dose FZKA decoction treatment of HO-8910PM cells, FN protein expression decreased significantly (P<0. 05 or P< 0. 01). Compared with the control group, after 24 h of low -, medium- and high-dose FZKA decoction treatment of HO-8910PM cells, E-cadherin mRNA expression increased (P<0. 01), while vimentin, N-cadherin mRNA, TGF-β1, and p-SmaD₃ expression decreased significantly (P<0. 01). Conclusions FZKA can inhibit the migration and invasion of HO-8910PM cells, by inhibiting TGF-β1 / SmaD₃ pathway activation and further regulation of the EMT process.

Abstract: Objective To investigate the anti-asthmatic, anti-tussive, and expectorant effects of Tanchuanning mixture. Methods An Asthma model in rats was established by sensitization and challenge with ovalbumin (OVA) and then airway resistance (R_L ) was observed. Serum levels of IgE, IL-4, IL-17, and TNF-α were analyzed by ELISAs. The numbers of WBCs and EOSs in BALF of rats were counted and HE staining of lung tissue was performed to observe pathological changes. Methacholine chloride and histamine phosphate were used to induce asthma in guinea pigs to observe the anti-asthmatic effect of Tanchuanning mixture. The anti-tussive effect of Tanchuanning mixture was observed in a cough mouse model induced by ammonia and guinea pig model induced by citric acid. A phenol red excretion test in the tracheas of mice was used to observe the expectorant effect of Tanchuanning mixture. Results Tanchuanning mixture reduced airway resistance, decreased IgE, IL-4, IL-17, TNF-α levels in serum and the number of WBCs and EOSs in BALF, and alleviated lung tissue damage in asthmatic rats (P<0. 05 or P<0. 01). Tanchuanning mixture prolonged asthma and cough latencies in guinea pigs and mice, respectively, reduced the cough times in mice, and increased phenol red excretion in mice ( P< 0. 05 or P< 0. 01 ). Conclusions Tanchuanning mixture has obvious anti-asthmatic, anti-tussive, and expectorant effects.

Abstract: Objective To establish the H1299 cell line with HNRNPK downregulated by DOX and study the effect of HNRNPK downregulation on cell proliferation and apoptosis. Methods H1299 cells were infected with a packaged lentivirus. After 72 h, positive cells were selected by puromycin and expanded to a stable transgenic cell line. The expression efficiency of HNRNPK was detected by qPCR and Western blot. The effects of HNRNPK downregulation on cell proliferation and apoptosis were analyzed. Results The H1299 cell line with HNRNPK downregulated by DOX was established successfully. Downregulation of HNRNPK inhibited the proliferation of H1299 cells but did not affect apoptosis. Conclusions Downregulation of HNRNPK inhibits the proliferation of H1299 cells.

Abstract: Objective Circulating miR-29b has been rEPORted to be positively correlated with nonalcoholic fatty liver disease (NAFLD). However, the role of miR-29b-3pI in NAFLD progression is unclear. The purpose of this study was to evaluate the expression of miR-29b-3p in NAFLD models and to identify the potential functions of miR-29b-3p in lipid accumulation and fibrosis in hepatocytes. Methods Palmitic acid (PA)-treated L02 cells were used as an in vitro cellular model of NAFLD. miR-29b-3p and insulin-like growth factor-1 (IGF-1) expression levels were determined by RT-qPCR or Western blot. miR-29b-3p mimic / inhibitor or IGF-1 siRNA were transfected into L02 cells exposed to PA. Lipid accumulation was determined by oil red O staining, and triglyceride and total cholesterol assays. Direct interaction between miR-29b-3p and IGF-1 was determined by dual-luciferase reporter assay. Results The result revealed that miR-29b-3p was upregulated in our in vitro cellular model of NAFLD while IGF-1 concentrations decreased. miR-29b-3p inhibition significantly suppressed lipid accumulation and fibrosis in PA-treated L02 cells. miR-29b-3p targets IGF-1 and suppresses its expression in vitro. Interestingly, the effects of miR-29b-3p overexpression on lipid accumulation and fibrosis in PA- treated L02 cells was enhanced by IGF-1 silencing. Conclusions Our result suggested that miR-29b-3p has a negative regulatory effect on lipid accumulation and fibrosis in hepatocytes by targeting IGF-1. This study provides evidence that miR-29b-3p might be a promising therapeutic target for NAFLD.

Abstract: Objective To investigate the effect of propofol on cerebral ischemia-reperfusion injury in rats through the Rho / Rho kinase signaling pathway. Methods One hundred SD rats were divided into control, model, and propofol low, medium, and high dose (20, 40, and 80 mg / kg) groups. Rats in the model and propofol low, medium, and high dose groups were used to establish a cerebral ischemia-reperfusion injury model. After successful modeling, rats in propofol low, medium, and high dose groups were administered the corresponding dose of propofol and rats in control and model groups were administered the same volume of normal saline for 4 weeks. Then, each rat was scored for neurological deficits, stickers were removed, and balance beam walking experiments were performed. Pathological scores in the hippocampus of rats were calculated. Rho and Rho kinase mRNA and protein levels were determined in rat brain tissue. Results The neurological deficit score, bilateral sticker removal time, balance beam time, pathological score of the hippocampus, and Rho and Rho kinase mRNA and protein expression levels in the model group were significantly higher than those in the control group (P<0. 05). The neurological deficit score, bilateral sticker removal time, balance beam time, pathological score of the hippocampus, and Rho and Rho kinase mRNA and protein expression levels in all propofol groups were significantly lower than those in the model group (P<0. 05). With the increase of the propofol dose, the neurological deficit score, the time of side sticker removal, balance beam time, pathological score of the hippocampus, and Rho and Rho kinase mRNA and protein expression levels were decreased gradually and dose-response relationships were obvious (P< 0. 05). In the control group, neuronal cells were intact with a normal structure, clear staining, and oval nucleus in the center. In the model group, a large number of necrotic neurons were seen with obvious cell loss and nuclear pyknosis. In the high dose propofol group, a small number of necrotic neuronal cells were seen, the neuronal cell structure was relatively complete, and the nuclei of neurons were oval in the center. Compared with the model group, the numbers of necrotic neurons were decreased in middle and low dose propofol groups, but the meridians were loose and disordered, the nucleus exhibited pyknosis, and loss was obvious. Conclusions Propofol reduces neurological damage in rats with cerebral ischemia-reperfusion injury. The mechanism is related to inhibition of Rho and Rho kinase mRNA and protein expression by propofol and thus inhibition of activation of the Rho / Rho kinase signaling pathway.

Abstract: Objective To study the modeling elements of rheumatoid arthritis (RA) animal models and provide a method ological reference to improve the success rate of modeling and evaluate the effectiveness of tested drugs. Methods Rheumatoid arthritis and animal models were used as subject headings and the relevant journal documents of CNKI and Wanfang databases (January 2017 to December 2019) were searched. The experimental animal species, excitation method, inflammatory method, and detection indexes were collected and a database was established. Excel 2012 and SPSS Statistics 19. 0 statistical software were used to carry out association rule and factor analyses of imported traditional Chinese medicine. Statistical analysis was also carried out. Results A total of 259 periodicals were included, among which male SD rats (69 times, 25. 18%) and male Wistar rats (54 times, 19. 71%) were the most frequently used experimental animals. The most frequently used inflammatory method were CIA (172 times, 62. 77%) and AA (82 times, 29. 93%). The most frequently used stimulation method were subcutaneous injection of the tail root (71 times, 25. 91%) and intradermal injection of the right hind foot (52 times, 18. 98%). The most frequently detected indexes were the swelling degree of the foot sole (133 times, 17. 48%), arthritis score index ( 84 times, 11. 04%), serum TNF-α level ( 74 times, 9. 72%), and joint histopathology (66 times, 8. 67%). Conclusions The result suggested the use of male SD or Wistar rats to induce inflammation by subcutaneous injection at the tail root when establishing animal models of rheumatoid arthritis. The success rate of the model can be improved using 0. 1 ml emulsion mixed with bovine type II collagen and Freund’ s incomplete or complete adjuvant at 1∶1. After consulting the literature in the past 3 years, 274 articles meeting the requirements were selected. This study analyzed the existing animal models, provides suggestions to improve animal models of rheumatoid arthritis and standardize model evaluation, improves the coincidence degree between animal models and the clinic, summarizes the research progress of animal models of rheumatoid arthritis from the aspects of model animal selection, types of rheumatoid arthritis models, modeling drugs and detection indexes, and promotes in-depth research of rheumatoid arthritis.

Abstract: Objective To study the correlation between vascular calcification and serum bone metabolism markers in rats with chronic kidney disease. Methods Thirty six male SD rats were randomly divided into a control group ( 18 rats) and CKD vascular calcification group (18 rats). The calcification group was administered adenine combined with high phosphorus feed and the control group was administered normal saline and common feed. The rats were sacrificed after 2, 4, and 6 weeks and the aorta was collected for Von Kossa staining and calcium content analysis to detect the degree of calcification. Blood and urine were collected to detect urea nitrogen (BUN), blood creatinine (Scr), and bone metabolism markers calcium (Ca), phosphorus (P), 1,25-dihydroxy vitamin D₃ [1,25 (OH)₂D₃ ], parathyroid hormone (PTH), bone alkaline phosphatase ( BALP), osteocalcin ( OC), total type I procollagen amino terminal peptide ( tPINP), β- carboxy-terminal peptide of type I collagen (β-CTX), tartrate-resistant acid phosphatase-5b (TRACP-5b), and 24-hour urinary protein (24 h-Upro). Results Aortic Von Kossa staining showed no black matter deposition at each time point in the control group, whereas black matter deposition in the CKD vascular calcification group was increased gradually over time. Compared with the control group, the contents of BUN, Scr, 24 h-upro, and aortic calcium were increased in the CKD vascular calcification group (P<0. 05). Ca, 1,25(OH)₂D₃ , PTH, tPINP, β-CTX, and TRACP-5b were decreased (P<0. 05), P and Ca?P were increased (P<0. 05), and BALP and OC were also increased (P>0. 05). Binary logistic regression showed that increased serum Ca ? P and decreased PTH and TRACP-5b were independent risk factors for vascular calcification. In accordance with the degree of aortic calcification, the CKD vascular calcification group was further divided into two subgroups: mild-moderate calcification (2 and 4 weeks) and severe calcification (6 weeks). Compared with the mild- moderate calcification group, the contents of BUN, Scr and, aorta calcium were increased in the severe calcification group, (P<0. 05), while 24 h-upro was increased (P>0. 05). Ca, P, 1,25(OH)₂D₃ , tPINP, and TRACP- 5b were also increased (P>0. 05), while Ca?P, PTH, BALP, and β-CTX were increased (P< 0. 05), and OC was decreased (P<0. 05). Analysis of risk factors for the severity of vascular calcification revealed that increased serum Ca?P and decreased OC were independent risk factors for the severity of vascular calcification. Correlation analysis showed that serum Ca ? P, PTH, BALP, and β-CTX levels were positively correlated with vascular calcification, and OC was negatively correlated with vascular calcification. Conclusions Vascular calcification in CKD rats is closely related to bone metabolism. Detection of serum markers of bone metabolism is helpful to assess the occurrence of vascular calcification and judge the severity and progression of vascular calcification.

Abstract: Objective To investigate the effect of Yupingfeng powder on the expression of retinoic acid-related orphan nuclear receptor γt (RORγt) and related factors in experimental allergic rhinitis (AR) rats. Methods Forty SD rats were randomly divided into a normal group, model group, Yupingfeng group, and cetirizine group, with 10 rats in each group. The AR rat model of allergic rhinitis was established using the egg albumin sensitization method . The Yupingfeng powder doses were calculated according to the rats’ weights as the Yupingfeng group, 10 g / kg and cetirizine group, 2 mg / kg. The normal group and the model group were given the same amount of physiological salt by gavage, and the secretion levels of cytokines IL-17, TNF-α, IL-23, and IL-6 in the rats’ nasal mucosa in each group were detected by ELISA. H&E staining was used to detect the degree of damage to the nasal mucosal tissues in each group. The expression of ROR Tprotein in rat nasal mucosa was detected by immunohistochemistry. The mRNA expressions of RORγt, IL-17, and IL-23 in the nasal mucosa of the rats in each group were detected by RT-PCR. Results Compared with the normal group, nasal symptom scores, nasal mucosal thickness, expression levels of cytokines IL-17, TNF-α, IL-23, and IL-6, and the mRNA levels of RORγt, IL-17, and IL-23 were significantly increased in the model group (P<0. 05). Compared with the model group, values for the above indices in the Yupingfeng group and cetirizine group were significantly lower ( P < 0. 05). Conclusions Yupingfeng powder can regulate the expression of ROR T and the related factors, IL-17 and IL-23, and play an immunomodulatory role in AR.

Abstract: Objective To identify the prevalence of ECTV in mice. Methods A sensitive and specific FQ-PCR assay for ECTV was developed and used to detect and quantitate ECTV in mouse samples by analyzing the sequence of the crmD gene in ECTV. Results This assay detected a minimum of 10 copies of standard DNA. The assay was applied to 63 naked mole rat spleen samples and 22 mouse spleen samples raised in the laboratory, which provided negative result . In tissue samples from four ground squirrels raised in our laboratory, the positive rate was 50%. Some positive samples amplified with primers for the crmD gene had 99% similarities to ECTV as determined by sequencing the PCR products. Conclusions Our result suggest that routine surveillance of ECTV in laboratory mice cannot be ignored.

Abstract: Objective To evaluate the feasibility and safety of two different types of left atrial appendage occluder with a single disc cylinder or double disc device. Methods Fourteen healthy canines were subjected to left atrial appendage closure (LAAC) with the single disc cylinder or double disc device percutaneously. Closure was evaluated by left atrial angiography. The cause of death was analyzed by gross specimen examination of dogs that had died unexpectedly. The canines were sacrificed post-procedure at 45, 80, 110 days, and 15 months. Endothelialization of the device surface was evaluated by HE staining, immunofluorescence staining of CD31, and DAPI staining. Results Single disc cylinder devices were implanted in six canines, five of which died within 30 min to 8 h post-procedure, and one canine survived until 15 months. A large number of blood clots were formed on the device surface in four canines, and one-fifth of the device surface in the surviving canine was not covered by new tissue. Double disc occluders were implanted successfully in eight canines. The left atrial appendage of seven canines was sealed completely and a small residual shunt was observed in one canine immediately post-procedure. New tissue had covered the sealing disc completely on day 110. HE and immunofluorescence staining confirmed complete intima formation and neovascularization within 4 months. Conclusions The incidence of acute thrombosis and the mortality rate of LAAC with a single disc device were high. LAAC with double disc devices had less device-related complications and neointima formation was completed by 4 months post-procedure.

Abstract:Bronchial asthma is a chronic inflammatory disease characterized by airway inflammation, hyper- responsiveness, and remodeling, which are manifested as recurrent wheezing or coughing and chest distress. Recent studies indicate that lncRNAs and circRNAs competitively sponge miRNAs via microRNA response elements, form a competing endogenous RNA regulatory network, and therefore regulate post-transcriptional gene expression and play a major regulating role in the development and progression of asthma. This article reviews the mechanisms of ceRNA and its effects on asthma.

Abstract:Coronavirus disease 2019 (COVID-19), caused by infection with the novel coronavirus ( SARS-CoV- 2), was rEPORted in 2019. Subsequently, the outbreak spread rapidly in many countries and regions. COVID-19 is highly contagious and lethal, and detecting the novel coronavirus is essential to effectively control transmission during the pandemic. Research teams and institutions in China and abroad have developed various effective method and equipment to detect the new coronavirus, and in this article, we summarized the current main detection method and equipment while considering the principles, range of applications, and advantages and disadvantages.

Abstract:Annexin A2 (ANXA2) is a multifunctional calcium-dependent phospholipid-binding protein. Previous rEPORts have shown that ANXA2 is closely related to the occurrence and development of various tumors. However, knockdown, knockout or overexpression of ANXA2 using gene regulation technologies have indicated that ANXA2 is multifunction and involved in various pathological processes including cells proliferation, tumor cell invasion, neoangiogenesis, the plasmin system, inflammatory response, epithelial - mesenchymal transition, anti-cancer drug resistance, and side effects. It also participates in the occurrence and development of tumors and non-tumor diseases. These pathological effects and pathways of ANXA2 at the genetic level were summarized on the basis of recent developments and we also explored whether ANXA2 can be used as a target for eaR_Ly diagnosis and treatment of the related diseases.

Abstract:By consulting existing articles on animal experiments of yin deficiency syndrome, we considered that previous studies have involved kidney, lung, spleen, stomach, and liver yin deficiencies, and summarized the modeling method, general observation state, detection index, and drug reverse syndrome of animal models of yin deficiency to provide a reference to evaluate animal models of yin deficiency and direction to establish a more unified evaluation system.

Abstract:Yang deficiency is a common clinical syndrome in traditional Chinese medicine and is involved in many diseases, such as yang deficiency constitution, which is becoming more common. Furthermore, most late-stage disease will involve varying degrees of yang deficiency syndrome. Animal models of yang deficiency are mainly established according to three aspects: simulating the etiology of traditional Chinese medicine; western medicine pathology; and combining disease and syndrome, focusing on the spleen and kidney viscera. Studies of the essence and material basis of yang deficiency are performed according to two aspects: 1. physiological, biochemical, and molecular biology, including endocrine, immune, hemorheology, energy metabolism, free radicals, and trace elements; and 2. the level of genes, proteins, and metabolomics. These studies and method help us understand the pathogenesis of yang deficiency and its related diseases, perfect the diagnostic criteria of yang deficiency in different zang-fu viscera, and lay a foundation for the standardization of clinical treatment according to syndrome differentiation.

Abstract:In China, the incidence of gastric cancer has increased with the aging population, and this is a malignant cancer with high mortality. Currently, the lack of effective anti-tumor drugs is a key concern; therefore, preclinical research is crucial, and animal models are important. Modern research emphasizes precise tumor treatment, and patient-derived xenografts ( PDX) have emerged from related research. PDX are highly consistent with the biological characteristics of the original tumor, which addresses the deficiencies of the traditional cell line model and provides a new platform for tumor research. In this paper, we review the established method of PDX modelling for gastric cancer. We also summarize the related research and its application in recent years.

Abstract:Rheumatoid arthritis (RA) is a common autoimmune disease with high disability, and its pathological mechanism is still unclear. Therefore, it is of great significance to construct appropriate animal models, especially those similar to human RA, in the study of the pathogenesis and clinical treatment of RA. There are many strains and method of rats and mice to construct the rheumatoid arthritis model. In this paper, we review the rEPORted mature and stable rat and mouse models related to RA.