Abstract: Objective 　To investigate the mechanisms of macrophage activity in the process of myocardial regeneration and explore the feasibility of eliminating macrophages after constructing a myocardial infarction model in CD11b^DTR newborn mice. Methods 　CD11b^DTR mice were injected with DT to eliminate macrophages on their day of birth after ligation of the left anterior descending branch of the coronary artery. This established a myocardial infarction model with macrophage elimination to explore the role of macrophages in the process of myocardial infarction. Results 　After ligating the left anterior descending branch of the coronary artery of CD11b^DTR mice on their day of birth to construct the myocardial infarction model, DT injection failed to significantly eliminate their macrophages. Macrophages could not be eliminated by increasing the administration frequency or concentration. Increasing the administration frequency and concentration at the same time had an obvious macrophage elimination effect, but the survival rate of the DT group mice decreased significantly, and the survival state of the surviving mice was very poor. Thus, this method cannot be used for subsequent experiments. Conclusions 　Mice injected with DT under physiological conditions showed significant macrophage elimination in the heart. However, after coronary artery ligation of CD11b^DTR mice to create a myocardial infarction model, macrophage elimination could not be obtained by injecting DT, which may be caused by the fact that coronary artery ligation prevented the DT from being delivered to the heart normally, preventing it from effectively acting on macrophages in this organ.

Abstract: Objective 　To explore the role and activity mechanisms of demethylase JARID1D in the invasion and metastasis of prostate cancer in order to provide new predictive indicators and therapeutic targets for the metastasis of prostate cancer. Methods 　The prostate cancer cell lines 22RV1 and DU145 were transfected with lentivirus to knock down the expression of JARID1D. These cell lines were named sh-JARID1D. The change in JARID1D expression in sh-JARID1D cells was confirmed by qRT-PCR and Western Blot. Changes in cell invasion ability after decreasing JARID1D expression were detected by Transwell experiment. An experimental metastasis animal model was established by injecting sh-JARID1D cells into the tail vein of nude mice, and changes in tumor cell metastasis ability were evaluated in vivo after knockdown of JARID1D expression. The effect of JARID1D on metastasis-related gene matrix metalloproteinase 2 (MMP2) was detected by qRT-PCR and Western Blot. Results 　The Transwell experiment showed the increased invasion ability of prostate cancer cells after JARID1D knockdown (22RV1 cell line P< 0. 01, DU145 cell line P< 0. 001). We also found that low expression of JARID1D significantly enhanced the metastatic potential of tumor cells in nude mice (22RV1 metastasis model P< 0. 01, DU145 metastasis model P< 0. 01). Further experiments demonstrated that reducing the expression of JARID1D promoted the expression of MMP2. Conclusions 　Knocking down the expression of JARID1D increased the level of MMP2 in prostate cancer cells, promoting epithelial mesenchymal transition, enhancing the invasion and metastasis of prostate cancer, and thus affecting the progression of prostate cancer.

Abstract: Objective 　Three different method were used to establish rat models of psycho-cardiac disease(comorbidity of depression and cardiovascular disease). The characteristic changes in depressive behaviors, cardiac function, and related biochemical indicators were compared to provide a choice of relevant models for psycho-cardiac disease research. Methods 　Sixty male Sprague-Dawley rats were randomly divided into four groups. Rats in the control group were fed without special treatment; the ISO + CUMS group was intraperitoneally injected with isoproterenol and then subjected to chronic unpredictable mild stress for 4 weeks; the LAD + CRS group underwent left anterior descending coronary artery suture ligation surgery followed by chronic restraint stress for 4 weeks; the CORT group was given corticosterone aqueous solution (10 mg/ day) for 4 weeks. The depressive-like behavior of animals was evaluated in behavioral tests. Brain-derived neurotrophic factor levels in the hippocampus were analyzed by ELISA. Plasma corticosterone levels were determined by radioimmunoassay. Cardiac function was evaluated by ultrasound. Glucocorticoid receptor levels in myocardial tissue were determined by western blot. Masson staining was utilized to assess rat myocardial tissue fibrosis. Results 　All three modeling method successfully induced depressive-like symptoms and showed changes in cardiac structure and cardiac function compared with the control group. The ISO + CUMS and LAD + CRS groups showed more obvious cardiac structural changes and decreased cardiac function than the CORT group. Animals in the CORT group had higher levels of circulating corticosterone. Conclusions 　Corticosterone administration induces an effective and simple psycho-cardiac model with obvious hypothalamic-pituitary-adrenal axis dysfunction. Isoprenaline administration plus chronic unpredictable mild stress and coronary artery suture ligation surgery plus chronic restraint stress induced more obvious changes in cardiac function. This study provides a reference for the selection of animal models for studies into the mechanisms of psycho-cardiac disease, drug screening, and pharmacodynamic evaluation.

Abstract: Objective 　To provide a basis for the model in this paper, we analyzed the characteristics of acute myocardial ischemia (AMI) models and relevant phenotypic indexes in the literature. Methods 　In the literature research, the time range was January 2001 to December 2021; “acute myocardial ischemia” and “animal experiments” were used as the subject search terms, and Web of Science, China Knowledge Network, Wanfang, and Weipu databases were searched to summarize the characteristics of AMI modeling and phenotypic indicators. In the animal experiments, 40 healthy 5- to 6-week-old SPF SD rats, both male and female, were randomly divided into four groups (sham male, sham female, coronary artery ligation (LAD) male, and LAD female), with 10 rats in each group. LAD group underwent ligation of the left anterior descending coronary artery ( LAD), Sham group underwent the same operation, but only threading without ligation. Powerlab was used to monitor electrocardiogram (ECG) changes, and HE staining was used to observe myocardial pathological changes. ELISA was used to detect serum cardiac enzymes (CK-MB, cTnI) and oxidative stress factors(MDA, SOD, Uch-L1) in the hippocampal CA1 region. The levels of apoptotic proteins (Caspase-3, PARP1, Cleaved Caspase-3, Cleaved PARP1) in the hippocampal CA1 region were detected by Western Blot. Results 　An analysis of 411 papers found that most studies selected SD or Wistar rats to prepare LAD models and concentrated on morphological and functional changes to the heart, while studies on heart-brain crosstalk were rare. Compared with the sham-operation groups, LAD male and female rats showed a significantly elevated ST segment on ECG, cardiac myocyte edema, disturbed myocardial fiber sorting, extensive inflammatory cell infiltration, and expression of serum CK-MB, cTnI, and Uch-L1. The expression of MDA, Cleaved Caspase-3/ Caspase-3, and cleaved PARP1/ PARP1 was increased and SOD was significantly decreased in the CA1 region of the rat hippocampus. Conclusions 　Acute myocardial ischemia can cause hippocampal oxidative stress and induce neuronal apoptosis, and cardiovascular disease is potentially associated with brain dysfunction.

Abstract: Objective 　To determine the appropriate dose of bleomycin to induce pulmonary fibrosis in rat and mice models via a single intratracheal instillation and to compare model characteristics. Methods 　Thirty SD rats were randomly divided into blank group, bleomycin low-dose group (3 mg/ kg, BL-L group), bleomycin high-dose group (5 mg/ kg, BL-H group), 10 in each group, and 30 C57BL/6J mice were grouped as above. The animals’ general condition and body weight changes were observed. The tidal volume (TV), minute ventilation (MV), and 50% tidal volume expiratory flow (EF50) of rats and mice were measured with an animal lung function instrument. HE and Masson’s staining were used to observe histological changes to the lung tissues. Lung collagen content was measured with a hydroxyproline (HYP) kit. Results 　In the BL-L and BL-H groups, the survival rates of C57BL/6J mice were 70% and 80% and those of SD rats were 70% and 50%, respectively. From day 7, there was a significant decrease in the body weight of C57BL/6J mice in the BL-H group (P< 0. 05, P< 0. 01) and SD rats in the BL-L and BL-H groups (P< 0.01). Compared with the blank group, TV was decreased in SD rats in both dose groups (P < 0. 01) on day 10, but no significant change was observed in C57BL/6J mice. On day 21, lung function TV and MV were significantly decreased in the BL-L group rats (P< 0. 05, P< 0. 01); TV was significantly decreased in the BL-H group rats (P< 0. 01); and TV, MV, and EF50 were significantly decreased in C57BL/6J mice in both dose groups (P< 0. 05, P< 0. 01). In the lung tissues of C57BL/6J mice and SD rats in the BL-L and BL-H groups on day 21, inflammatory infiltration and fibrous cords appeared, alveolitis and fibrosis degree scores were significantly increased (P< 0. 05, P< 0. 01), and HYP levels were significantly increased (P< 0. 05, P< 0. 01). Conclusions 　Both 3 mg/ kg and 5 mg/ kg bleomycin induced pulmonary fibrosis models in rats and mice. Based on survival rate, lung function, lung pathology, and other indicators, the optimal dose for C57BL/6J mice was 5 mg/ kg and that for SD rats was 3 mg/ kg.

Abstract: Objective 　To explore the formation conditions and phenotype of a mouse model of liver fibrosis induced by HBV (hepatitis B virus,HBV)infection. Methods 　Eighteen CBA/ CaJ mice were randomly divided into control group (n= 4) and experimental group (n= 14), and the experimental group was injected with cccDNA by tail vein at a dose of 2 μg per mouse by high-pressure hydrodynamic method, and the control group was injected with an equal volume of PBS. Samples were obtained 68 weeks after transfection. HBV DNA and HBV cccDNA in mouse livers were detected by quantitative PCR. Serum HBsAg (hepatitis B surface antigen,HBsAg) and HBeAg (hepatitis Be antigen, HBeAg) levels were tested using ELISA. HBsAg and HBcAg liver tissue levels were tested by immunohistochemistry. HBV DNA in mouse liver tissue, with the phenotype HBeAg+ / HBsAg- or HBeAg^- / HBsAg⁺ , were first-generation sequenced. ALT and AST levels were evaluated by biochemical analysis, and histopathology was analyzed by HE, Sirius, and Masson staining. Results 　In the experimental group, 100% of mouse HBV DNA was higher than 1000 copies/ mL. The cccDNA copy number of mouse liver tissue was significantly higher than that of the blank group (P< 0. 05); 42. 9% of mice were positive for HBsAg and HBeAg, 60% were positive for HBsAg, and 26. 7% were positive for HBcAg. Mutations at A1762T/ G1764A and G1896A/ G1899A were found in HBeAg^- / HBsAg⁺ samples, and there were multiple mutations in the S2 and S regions of HBeAg+ / HBsAg- samples. ALT and AST values were abnormal in 57. 1% and 7. 1% of mice, respectively. Liver damage and infiltration were observed in all experimental mice, and liver tissue fibrosis was found in 92. 9% of mice. Conclusions 　HBV DNA、HBV cccDNA、HBsAg、HBeAg of Serum and liver tissue remained positive 68 weeks after hydrodynamically injecting HBV cccDNA into CBA/ CaJ mice. HBV infection caused liver fibrosis in mice and even mimicked a clinical HBV BCP/ PC gene mutation phenotype.

Abstract: Objective 　To explore Methods of streptozotocin-induced diabetic pulmonary fibrosis mouse model establishment and provide a stable animal model of diabetic pulmonary fibrosis for clinical research. Methods 　Sixty male C57BL/6 mice were randomly divided into three groups: normal control (NG, n= 20), diabetic pulmonary fibrosis 1 (DPF1, n= 20), and diabetic pulmonary fibrosis 2 (DPF2, n= 20) groups. The fasting blood glucose levels and body weight of the mice were measured after overnight fasting; then the DPF1 group was intraperitoneally injected with a large dose of streptozotocin (150 mg/ kg), and the DPF2 group was intraperitoneally injected with a small dose of streptozotocin (50 mg/ kg) every day for five consecutive days. The NG group was intraperitoneally injected with the same amount of sterile citrate buffer. After injection, the general condition of the mice was observed every day, and the body weight and random blood glucose of the mice were measured every week. The mice were fed normally for 16 weeks, and five mice were randomly selected from each group every 4 weeks to be sacrificed for pathology and molecular biology assays to assess the degree of pulmonary fibrosis. Results 　After streptozotocin induction, both the DPF1 and DPF2 groups had typical symptoms of diabetes including polydipsia, polyuria, polyphagia and weight loss. The body weight of the DPF1 and DPF2 groups increased slower than that of the NG group, and gradually decreased from the 8th week (P< 0. 05). The random blood glucose of the DPF1 and DPF2 groups was greater than 16. 7 mmol/ L after the 1st week and the 2nd week, respectively, and tended to be stable after the 9th week (P< 0. 05). The pathological results showed that, compared with the NG group, the DPF1 and DPF2 groups had no obvious fibrotic lesions at 4 weeks. However, a small number of fibrotic lesions were observed around the vessels at 8 weeks. Obvious fibrotic lesions were observed at 12 weeks, mainly accumulated around the blood vessels; and more obvious fibrotic lesions were observed at 16 weeks that involved the surrounding lung tissue. The molecular biological results were similar to the pathological results . Compared with the NG group, the DPF1 and DPF2 groups’ expression levels of mouse fibrosis marker collagen 3 did not change significantly at 4 and 8 weeks, but increased at 12 weeks (P< 0. 05) and significantly increased at 16 weeks (P< 0. 05). Conclusions A single high-dose intraperitoneal injection of streptozotocin (150 mg/ kg) and five consecutive low-dose intraperitoneal injections of streptozotocin (50 mg/ kg) induced diabetic pulmonary fibrosis mouse models after 16 weeks of feeding, and both produced ideal animal models for diabetic pulmonary fibrosis.

Abstract: Objective 　To compare the effects of intra-tracheal drip and intratracheal nebulized spray of bleomycin (5 mg/ kg) on the rat model of pulmonary fibrosis, and to compare the effects of intraperitoneal 3% pentobarbital sodium anesthesia and isoflurane respiratory anesthesia (isoflurane concentration of 0. 5% when mixed with oxygen for inhalation) on the rat model of pulmonary fibrosis, and to explore a more optimal modeling method. Methods 　 Fifty male SPF-grade SD rats were randomly divided into blank control group, intraperitoneal anesthetic intratracheal drip group, intraperitoneal anesthetic intratracheal nebulizer spray group, respiratory anesthetic intratracheal drip group and respiratory anesthetic intratracheal nebulizer spray group, 10 rats in each group. The survival status and body weight of rats in each group were observed at 1, 3, 7, 14 and 21 d after drug administration; rats were executed 3 weeks after drug administration, and lungs were weighed to calculate lung coefficients; HE staining was performed to observe inflammatory changes in lung tissues; Masson staining was performed to observe collagen proliferation in lung tissues; Western Blot was performed to detect transforming growth factor-β1 (TGF-β1) protein expression in lung tissues; alkali hydrolysis was performed to detect hydroxyproline (HYP) in lung tissues. Results 　Compared with the blank control group, the rats in the four model groups had poor mental status, decreased body weight, and increased lung index; lung tissue damage was evident, increased inflammation levels, and significant collagen proliferation; increased TGF-β1 protein expression levels in lung tissues (P<0. 001); and increased hydroxyproline levels in lung tissues of rats in the intratracheal nebulizer sprayed with bleomycin only group were found ( P< 0. 05). The modeling approach of intratracheal drip injection was found to have a heterogeneous distribution of fibrotic lesions in the lungs of its model rats, with varying degrees of fibrosis. The mean time to awakening and mortality rates were lower in rats under isoflurane respiratory anesthesia (0. 5% isoflurane concentration when mixed with oxygen for inhalation) than in the intraperitoneal 3% pentobarbital sodium anesthesia modality when both anesthesia levels were medium. Conclusions 　Intratracheal nebulized spray of bleomycin under isoflurane respiratory anesthesia is the preferred modeling method for establishing a rat model of pulmonary fibrosis.

Abstract: Objective 　A PCR array was used to explore the effects of pyroptosis on extensor digitorum longus(EDL) loss in aging rats after a 32 weeks weight-bearing running regime. Methods 　Ninety SD rats were randomly divided into three groups: control group (C0 group, n= 10), aging no exercise group (C group, n= 40), and aging weightbearing running group (R group, n= 40). After 8, 16, 24, and 32 weeks of intervention, the C and R groups were divided into C8 group, C16 group, C24 group, C32 group, R8 group, R16 group, R24 group, R32 group (n= 10). After the intervention, the body weight, lean body mass, and EDL wet weight were measured. HE staining was used to observe the shape of muscle fibers, and the fiber cross-sectional area (FCSA) was calculated. The expression of key pyroptosis proteins, NF-κB, ASC, GSDMD, and Caspase1, were tested by Western Blot. Differentially expressed genes of pyroptosis of EDL were screened by PCR array, and the accuracy of the array result were verified by qPCR. Results 　(1) Body weight continued to increase in the C group, while that in R group was relatively stable. The lean body mass and its percentages were significantly lower in the C32 group than the C0 group. The lean body mass percentages were significantly higher in the R8, R24, and R32 groups than their corresponding C groups (P< 0. 05). (2) EDL wet weight and FCSA were significantly higher in the R24 and R32 groups than the C24 and C32 groups. The FCSA of each C group was lower than that of the C0 group (P< 0. 05). (3) The contents of NF-κB and GSDMD in the C16 and C24 groups; that of ASC in the R16 group; and that of Caspase1 in the C8, C16, C24, and R8 groups were significantly higher than those in the N group (P< 0. 05). The contents of NF-κB in the R16 and R24 groups, ASC and GSDMD in the R16 group, and Caspase1 in R group were lower than those in the respective C groups (P< 0. 05). (4) The PCR array showed that the expression of pyroptosis genes gradually decreased in the R group with training time. The downregulation of Naip6 and the key pyroptosis gene Casp1 in the R16/ C16 and R32/ C32 groups was verified by qPCR and was consistent with the array result. Conclusions 　32 weeks of weight-bearing running alleviated muscle loss in aging rats by inhibiting pyroptosis.

Abstract: Objective 　To investigate the regulatory effect of Lizhong pills on the IL-22-MUC2/ claudin-2 signaling pathway in the colonic mucosa of spleen-deficiency diarrhea rats. Methods 　A spleen-deficiency diarrhea rat model was established using a 1. 2 g/ mL decoction of senna leaf combined with fatigue swimming. Model rats were randomly divided into a model, montmorillonite powder (0. 9 g/ kg), and Lizhong pill low-dose and high-dose groups (0. 81, 3. 24 g/ kg), with eight rats in each group, and eight rats were selected for a blank group. The drugs were continuously administered for 14 days. After modeling, the rats had lost weight and displayed mental fatigue, squinting, less movement, soft or loose stools, and filth around the anus, indicating that the model was successfully replicated. Serum amylase and D-xylose levels were detected by colorimetry, and colonic mucosal morphology was detected by Alcian blue and periodic acid Schiff (ABPAS) staining. A Western Blot was used to detect the expression of aquaporin 3/4 (AQP3, AQP4), and Real-time fluorescence quantitative PCR to detect the relative expression levels (2^-ΔΔCt value) of interleukin-22 (IL-22) and claudin-2 genes. An immunofluorescence method was used to detect IL-22 and claudin-2 proteins in the colon tissue. Results Compared with the blank group, the model group rats had significantly increased defecation rate, defecation grade, and diarrhea index. Epithelial cells in the colon tissue of the model group were atrophied to varying degrees; the mucosal surface structure was loose and edemic, and the goblet cells had decreased in number. The serum amylase and D-xylose contents and the expression of AQP3 and AQP4 proteins in the colon tissue were decreased, while the protein and mRNA expressions of IL-22 decreased, and those of claudin-2 were increased in the model group. Compared with the model group, the high-dose Lizhong pill group displayed significantly reduced loose stool rate, loose stool grade, and diarrhea index; significantly reduced pathological damage to the colon mucosa; increased serum amylase and D-xylose contents; increased expression of AQP3 and AQP4 proteins, increased IL-22 mRNA, and decreased claudin-2 mRNA and protein in the colon tissue, and the differences were statistically significant (P< 0. 05 or P< 0. 01). Conclusions 　Lizhong pills significantly improved the structure and function of the colonic mucosal barrier in spleen-deficiency diarrhea rats, and the mechanism may be related to an increase in AQP3/4 expression and regulation of the IL-22-MUC2/ claudin-2 signaling pathway.

Abstract: Objective 　To explore the therapeutic effects and potential activity mechanisms of intestinal flora on a 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced intestinal fibrosis rat model. Methods 　24 SD rats were randomly divided into normal control, model, lincomycin hydrochloride (85 mg/ kg), and probiotic (850 mg/ kg) groups. Except for the normal control and model groups, which were given equal volumes of normal saline, the groups were given corresponding drugs by gavage, once a day, for five consecutive days. The next day, TNBS was used to induce the rat intestinal fibrosis model in all groups except for the normal control group. The corresponding drugs were then given for 7 d. During the experiment, the general behavior of the rats was observed. After the experiment, colonic specimens were collected for histological scoring. HE and Masson staining were used to observe the degree of colon tissue damage and fibrosis. The immunohistochemical detection of E-cadherin, α-SMA, TGF-β1, and other proteins and the Western Blot detection of TL1A and DR3 proteins were carried out. Results 　Compared with the normal control group, the model group rats’ colons were damaged, and the number of collagen fibers increased, indicating that the intestinal fiber model was successful. Lincomycin hydrochloride further aggravated colonic injury and collagen fiber expression, and colonic injury and fibrosis were alleviated by probiotic treatment. Compared with the model group, the lincomycin hydrochloride group had increased expression of TL1A/ DR3 protein (P< 0. 05) and decreased expression of E-cadherin, α-SMA, and TGF-β1 proteins (P< 0. 05). However, the probiotics group had significantly reduced protein expression levels of TL1A/ DR3, α-SMA, and TGF-β1, and increased levels of E-cadherin. Conclusions 　Microflora disorder promotes fibrosis by activating TL1A/ DR3 signaling to regulate epithelial mesenchymal transformation in colon tissue, and probiotic intervention can alleviate colonic fibrosis.

Abstract: Objective 　To explore the mechanisms involved in Xiangsha Liujunzi Tang intervention for functional dyspepsia (FD) in rats with spleen and stomach weakness via the CaM/ MLCK/ MLC20 pathway. Methods 　60 SPF male SD suckling rats were randomly divided into blank (n= 10) and modeling (n= 50) groups. A comprehensive modeling method (gavage administration of iodoacetamide + exhaustion of swimming + disturbance of hunger and satiety) was used to replicate an FD rat model with spleen and stomach weakness. After successful replication of the model, the rats in the modeling group were randomly divided into a model; positive control; and Xiangsha Liujunzi Tang high-, middle-, and lowdose groups, with 10 rats in each group. Rats in the blank and model groups were given 10 mL/ (kg·d) normal saline; the positive control group was given 1. 35 mg/ (kg·d) mosapride; and the high-, middle-, and low-dose Xiangsha Liujunzi Tang groups were given 12, 6, and 3 g/ (kg·d) Xiangsha Liujunzi Tang, respectively. The intervention lasted 14 days. The general condition of each rat was observed before and after modeling and administration, and food intake and body mass were measured. After the intervention, the gastric emptying rate and intestinal propulsion rate were measured, and pathological changes to gastric tissue were observed by hematoxylin-eosin staining. The content of Mg²⁺ -ATP enzyme in the gastric tissue was determined biochemically, and the protein expression levels of CaM, MLCK, and p-MLC20 in gastric tissue were detected by Western Blot. Results 　Compared with the blank group, the model group rats had withered hair; lazy movements; slow actions; significantly reduced general survival score; and lower food intake, body mass, gastric emptying rate, and intestinal propulsion rate ( P< 0. 05), but there was no obvious abnormality in their gastric histopathology. The content of Mg²⁺ -ATP enzyme in the gastric tissue decreased, and the protein expression levels of CaM, MLCK, and p-MLC20 in the gastric tissue decreased significantly. Compared with the model group, the high- and middledose group rats had significantly improved general survival status scores, while their food intake, body mass, gastric emptying rate, and intestinal propulsion rate were significantly increased ( P< 0. 05), but there was no significant difference in gastric pathology. The content of Mg²⁺ -ATP enzyme and the protein expression levels of CaM, MLCK, and p-MLC20 in gastric tissue also increased significantly. The intervention effect of Xiangsha Liujunzi Tang was dose dependent. Conclusions 　Xiangsha Liujunzi Tang effectively improved the general condition and gastric motility of FD rats with spleen and stomach weakness. The specific mechanism may be related to the activation of the CaM/ MLCK/ MLC20 pathway in gastric tissue to regulate smooth muscle contraction and promote gastric motility.

Abstract:Because of their multiple advantages as mammalian models for molecular genetic manipulation, rodents have been widely used for experimental models of eye diseases. In recent years, scholars have proposed a variety of new method to quantify animal vision based on previous qualitative method. In this paper, we discuss the detection method used in animal visual electrophysiology and their application in rodent models.

Abstract:Cancer is a major threat to human life and health globally and is second only to cardiovascular disease in terms of morbidity and mortality. Cancer remains a focus of attention of health services worldwide. Good animal models can not only be used to study the occurrence, development, and biological mechanisms of cancer but also to screen anticancer drugs and gene therapies. In recent years, patient-derived xenograft (PDX) models have become a research hotspot due to their ability to preserve the microenvironment and histological characteristics of primary tumors. This review summarizes the method of PDX animal modeling and its application in oncology medicine, as well as its limitations, providing an important reference for the application of PDX models in the field of tumor therapy.

Abstract:At the present time, we are facing an increasing prevalence of hyperuricemia and gout worldwide. Worryingly, hyperuricemia is closely associated with the development of chronic kidney disease, hypertension, obesity, type 2 diabetes, and atherosclerotic heart disease. The mechanism of these diseases and their complications have not been fully clarified, and there still exist some limitations and delays in the research into new drugs. One important obstacle is that there are too many types of hyperuricemia and gout animal models, and thus we are lacking a standard method. Moreover, most models have some shortcomings regarding the persistence and stability of blood uric acid levels. In this review, we discuss the availability of animal models of hyperuricemia and gouty arthritis, the method of model establishment, and the histopathological changes in major visceral organs, to provide a detailed reference for the establishment of animal models and the study of pathogenesis.

Abstract:Sj?gren’s syndrome (SS), also known as primary Sj?gren’s syndrome (pSS), is a chronic systemic autoimmune disease that mainly involves the exocrine glands. Patients predominantly suffer from dry mouth and dry eyes, and some patients may develop systemic damage. The etiology and pathogenesis of pSS still remain unclear, and clinical treatments are scarce. Studying pSS using animal models is an effective way to elucidate the etiology and pathogenesis of this human disease; however, the result obtained from different animal models should be carefully evaluated. In this review, three classes of SS-like mice are discussed, with special attention given to the heterozygous variant mouse model to provide a guide to those studying pSS.

Abstract:Precocious puberty is a common endocrine disease in children. Animal experiments are essential in the study of the pathogenesis and drug treatment of precocious puberty. Therefore, establishing an appropriate animal model is a prerequisite for studying the condition. The pubertal development processes in rats and non-human primates are similar to those in humans, and the indications of gonadal development are clear. Rats and non-human primates are common animal models of precocious puberty. According to different research needs, there are many modeling method of precocious puberty, such as danazol, N-methyl-DL-aspartic acid, estradiol, high-fat feed, low-safety environment, light and melatonin, manganese exposure, environmental endocrine disruptors, brain radiation, and intracerebral drug injection. At present, vaginal opening time, vaginal smear and estrous cycle observations, serum sex hormone level determination, hypothalamic gene-level index detection, sexual organ detection, and others, are the most common indicators used to evaluate precocious puberty during animal experiments.