Abstract: Objective　To investigate damage of double-stranded DNA by methamphetamine (METH) in various types of nerve cells. Methods　For in vitro experiments, primary cortical neurons and HT-22, BV2, HMC3 and U-87 MG cells were treated with METH. Cell morphology was observed and γ-H2AX expression was detected by Western blot. For in vivo experiments, METH was administered to mice by intraperitoneal injection, and behavioral analysis was performed by the open field test. Morphological changes of neurons in the prefrontal cortex and hippocampus of were observed by HE staining. Double-stranded DNA damage was observed by immunofluorescence, and γ-H2AX expression was detected by western blotting. Results　In vitro, after treatment with METH, the morphology of primary cortical neurons, and HT-22, BV2, HMC3 and U-87 MG cells had obviously changed, the synapses of cells were shortened or disappeared, cell bodies had shrunk, and gaps were wider. γ-H2AX expression was significantly increased. In vivo, after administration of METH, compared with the saline group, the movement trajectory and distance were significantly increased in the METH group. HE staining showed that neurons in the prefrontal cortex and hippocampus were markedly edematous and eosinophilic, and some neurons had degenerated. Immunofluorescence showed that double-stranded DNA damage in neurons in the prefrontal cortex and hippocampus of the METH group was significantly increased, and the fluorescence intensity was significantly enhanced compared with the saline group. Western blot showed that γ-H2AX expression in the prefrontal cortex and hippocampus of the METH group was significantly increased compared with the saline group. Conclusions 　METH damaged doublestranded DNA in the nervous system. METH induced a significant increase in γ-H2AX expression in primary cortical neurons HT-22, BV2, HMC3 and U-87 MG cells, the prefrontal cortex, and hippocampus. This study provides a theoretical basis to elucidate the mechanism of METH-induced neurotoxicity.

Abstract: Objective 　To evaluate the feasibility of an animal model of simulated adenoid hypertrophy by combining animal models of allergic rhinitis and chronic pharyngitis. Methods 　A rat model of allergic rhinitis was established by basal sensitization through intraperitoneal OVA injection and nasal enhanced sensitization. A model of chronic pharyngitis was established simultaneously by a throat spray of ammonia, both models were combined into a rat model of simulated adenoid hypertrophy. The symptom performance of model animals was assessed by the animal behavioral score after modeling. Pathomorphological changes of nasal and pharyngeal mucosae and nasopharyngeal lymph nodes were observed by HE staining. The percentage of eosinophils was assess in rat whole blood. IL-4 and IgE levels in rat serum and mucosal tissue were measured by ELISA. Results　The behavior score, eosinophil percentage, and IL-4 and IgE levels in serum and tissue were increased compared with the control group (P< 0. 01). Compared with model group A, the eosinophil percentage and serum IgE level were increased in model group B (P<0. 01). In the model groups, nasal and pharyngeal mucosae and nasopharyngeal lymph nodes showed different degrees of disease-related histopathological changes. Conclusions　The rat model had symptom manifestations and pathological changes similar to adenoid hypertrophy. This animal model of simulated adenoid hypertrophy can be used as a combined animal model of allergic rhinitis and chronic pharyngitis, but requires further exploration and improvement.

Abstract: Objective　To predict the mechanism of Shenshuai Prescription (SSR) in chronic kidney disease(CKD)-related myocardial injury using network pharmacology and molecular docking method. Methods　We used the traditional Chinese medicine systems pharmacology database and analysis platform (TCMSP) and Herb herbal medicine identification database (http:/ / herb. ac. cn/ ), and the SwissTargetPrediction database to screen target information of active ingredients. We then used the UniProt database to screen for human targets and standard gene names. A drug active ingredient target network diagram was constructed using Cytoscape 3. 7. 2 software, and the GeneCards database was used to collect disease-related targets. The “ Shenshuai Recipe” against CKD myocardial injury gene target database was established using Venny 2. 1, and the STRING database was used to build the main component target interaction network and screen key targets. Cytoscape 3. 7. 2 software was imported for topology analysis and a protein-protein interaction network diagram was constructed. Finally, the DAVID platform was used for Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and Gene Ontology (GO) biological function annotation. Results　After screening, there were 252 active compounds in SSR and 649 common targets of SSR and CKD myocardial injury, among which AKT Serine/ Threonine Kinase 1 (AKT1), Tumor Necrosis Factor (TNF), Mitogen-Activated Protein Kinase 3 (MAPK3), and Vascular Endothelial Growth Factor A (VEGFA) may be important targets of SSR in treating CKD myocardial injury. GO analysis identified 1485 Biological process items, 176 Cell component items, and 386 Molecular function items, of which plasma membrane, cytosol, and cytoplasm had the largest number of enriched genes, and 313, 304, 276 genes were distributed respectively. KEGG analysis indicated that HIF-1α, Lipid and atherosclerosis, AGE-RAGE signaling path in diagnostic complexes, phosphoinositide 3-kinase (PI3K)-AKT, and insulin resistance pathways might be involved in the mechanisms of SSR in treating CKD myocardial injury. Conclusions　SSR might play a role in cardiorenal protection by participating in multiple mechanisms, including improving insulin resistance, improving lipid metabolism, antiatherosclerosis, and regulating the expression of inflammatory factors and vascular endothelial growth factor, with the PI3K/Akt and mitogen-activated protein kinase pathways being potentially important signal regulation pathways.

Abstract: Objective　To investigate the factors affecting the establishment of a mouse model of alcoholic liver injury. Methods　A total of 150 specific-pathogen-free male ICR mice were divided into three groups to study the possible influences of different experimental conditions, including modeling period, frequency, type, and dosage of modeling agent, and time interval between doses. Mice in the three groups received 60% ethanol and alcohol with 53% volume ratio by gavage at different doses, frequencies, and time intervals and the mortality rates were calculated. We also detected alanine aminotransferase (ALT) and aspartate transaminase (AST) serum levels and malondialdehyde (MDA), glutathione(GSH), and triglyceride (TG) levels in liver tissue homogenate. Liver pathology was examined in tissue sections. Results The mortality rates in the 1-day modeling and double-dose liquor modeling groups were 20% and 40%, respectively, and the mortality rates in the 4, 6, 8, and 12 h interval dosing groups were 40%, 20%, 10%, and 0%, respectively. Pathological indicators, including ALT, AST, MDA, GSH, TG, and tissue pathology worsened in line with shortening of the gavage interval and increased gavage dose. Conclusions 　The alcohol dose, length of the modeling period, and frequency of dosing affect the establishment of an alcoholic liver injury model in mice. We suggest that dosing mice with alcohol with 53% volume ratio　twice a day at 20 mL/ kg body weight or 10 mL/ kg body weight at 6 h intervals can successfully cause liver damage.

Abstract: Objective　To investigate the effect of HIV infection on inosine-5’-monophosphate dehydrogenase 2(IMPDH2) expression in the cerebral temporal cortex. Methods　Montreal Cognitive Assessment (MoCA) scores and magnetic resonance imaging were used to assess mild cognitive impairment in HIV-infected patients. In addition, the histologic structure of the temporal cortex in a rhesus macaque with chronic simian-human immunodeficiency virus (SHIV) KU-1 infection was examined using hematoxylin and eosin staining. Moreover, IMPDH2 protein expression levels in paired healthy and infected temporal cortex were examined using immunohistochemistry and Western blot. Finally, putative genes associated with IMPDH2 expression were investigated using protein-protein interaction network analysis. Results　HIV positive individuals had a thinner temporal cortex compared with healthy controls. In addition, the numbers of neurons in the temporal cortex were decreased and IMPDH2 protein levels were significantly lower in the infected monkey compared with healthy controls. Eight genes interacting with the IMPDH2 gene were identified. Conclusions　Downregulation of IMPDH2 protein in the temporal cortex might be involved in the pathogenesis of HIV-related neurocognitive disease.

Abstract: Objective 　To investigate the effect and mechanism of Nardosinone (Nar) in hypoxia-induced apoptosis of H9c2 cardiomyocytes meditated through the PI3K/ Akt/ mTOR pathway. Methods　Cobalt chloride (CoCl₂ ) was used to establish a hypoxic injury model in H9c2 cardiomyocytes. Cell proliferation was assessed by CCK-8 assays. Hoechst 33342 was applied to counterstain cells, and laser scanning confocal microscopy was used to observe apoptosis. The potential signaling pathway of Nar in treating IHD was predicted by network pharmacology. Western blot was used to detect expression of apoptosis-, autophagy-, and PI3K/ Akt/ mTOR pathway-related proteins. Results　The PI3K/ Akt/mTOR pathway is major signaling pathway in Nar treatment of IHD. Compared with the control group, CoCl₂ (400 μmol/ L)decreased cell proliferation, the Bcl-2/ Bax ratio, PI3K, Akt and mTOR protein phosphorylation levels, and P62 protein expression, while increasing nuclear apoptotic fragmentation, the LC3II/ LC3I ratio, and Cleaved-Caspase-3 and Beclin-1 protein expression (P<0. 05). Compared with the CoCl₂ group, Nar (50 μmol/ L) pretreatment significantly increased cell proliferation, alleviated nuclear apoptotic fragmentation, decreased Cleaved-Caspase-3 protein expression, increased the Bcl-2/ Bax ratio, and increased PI3K, Akt and mTOR phosphorylation levels and P62 protein expression. The LC3II/ LC3I ratio and the Beclin-1 protein expression were also decreased (P< 0. 05). Pretreatment with PI3K specific inhibitor LY294002 offset the effects of Nar on CoCl₂-induced apoptosis, PI3K/ Akt/ mTOR pathway-related proteins, and P62 protein expression, but had no effect on the LC3II/ LC3I ratio or Beclin-1 expression. Conclusions　Nar inhibited CoCl₂-induced H9c2 cardiomyocyte apoptosis by activating the PI3K/ Akt/ mTOR pathway, but probably alleviated the damage caused by excessive autophagy in cells through other pathways.

Abstract: Objective　To establish and evaluate a chronic model of atopic dermatitis (AD) induced by 2,4-dinitrochlorobenzene (DNCB) in Brown Norway rats. Methods　Brown Norway rats were randomly divided into negative, model, and tacrolimus groups. The ear skin of rats in model and tacrolimus groups were challenged by 0. 5% DNCB at days 1, 3, 7, 9, 12, 14, 16, 19, 21, 23 and 25. Rats in the control group were administered a substrate solution at the same volume at the same time points. Rats in the tacrolimus group were transdermally administered tacrolimus ointment for 25 collected and weighted after 26 days of modeling. Histopathological examination and toluidine blue staining of ear tissue were also performed. The IgE level in ear tissue was detected. Results　The ear thickness in model rats was significantly increased after 9 days of challenge by DNCB, while whereas inflammation score was remarkedly improved after 12 days and reached a peak at 16~25 days. The weight of ear tissue and the IgE level in the ear were increased at day 26 of challenge. Pathological changes, such as epidermal thickening, inflammatory cell infiltration, and mast cell infiltration, occurred in the model group. Tacrolimus significantly reversed these changes. Conclusions　Brown Norway rats challenged by DNCB develop stable AD-like symptoms, which are appropriate for pharmacological evaluation.

Abstract: Objective　To explore the influence of miR-486-5p on the malignant behavior of endometrial cancer(EC) cells and its targeted regulation of PTEN. Methods　The expression miR-486-5p and PTEN mRNA in EC tissues and cells was detected by qRT-PCR. The correlation between miR-486-5p and PTEN mRNA expression in EC tissues and the clinical characteristics of patients were analyzed. A dual luciferase reporter assay was performed to verify the relationship between miR-486-5p and PTEN. Ishikawa cells were separated into NC, NC inhibitor, miR-486-5p inhibitor, miR-486-5p inhibitor+si-NC, and miR-486-5p inhibitor+si-PTEN groups. Western blot was performed to detect expression of PTEN and PI3K/ AKT pathway-related proteins in cells. CCK-8 assays were performed to assess cell viability. Colony formation assays were used to examine the ability of cells to form colonies. Flow cytometry was performed to assess apoptosis, Scratch healing and transwell assays were applied to assess cell migration and invasion. Results　The miR-486-5p was highly expressed in EC tissues and cells, while PTEN mRNA was expressed at a low level (P<0. 05). miR-486-5p and PTEN mRNA expression in EC tissues was related to the tumor size, differentiation degree, International Federation of Gynecology and Obstetrics stage, and lymph node metastasis (P<0. 05). miR-486-5p in Ishikawa cells might negatively target and regulate PTEN expression. Compared with NC and NC inhibitor groups, cell viability at 48 and 72 h, scratch healing rate, and ratios of p-PI3K/ PI3K and p-AKT/ AKT of Ishikawa cells in the miR-486-5p inhibitor group were decreased (P<0. 05), the number of colonies formed and the numbers of migrating and invasive cells were decreased (P<0. 05), and the apoptosis rate was increased (P<0. 05). Compared with miR-486-5p inhibitor and miR-486-5p inhibitor+si-NC groups, cell viability at 48 and 72 h, scratch healing rate, and ratios of p-PI3K/ PI3K and p-AKT/ AKT of Ishikawa cells in the miR-486-5p inhibitor+si-PTEN group were increased (P< 0. 05), the number of colonies formed and the numbers of migrating and invasive cells were increased (P<0. 05), and the apoptosis rate was decreased (P<0. 05). Conclusions　Inhibition of miR-486-5p may suppress activation of the PI3K/ AKT pathway by negatively targeting PTEN, thereby inhibiting the proliferation, migration, and invasion of EC cells and inducing their apoptosis.

Abstract: Objective　To explore how miR-34a-5p regulates insulin-like growth factor Ⅱ mRNA-binding protein 3 (IMP3) and programmed death ligand-1 (PD-L1) expression and its influence on the biological behavior of breast cancer cells. Methods　We analyzed IMP3 and PD-L1 expression in breast cancer and normal tissues using the Human Protein Atlas and GEPIA, and patient prognosis and survival using The Cancer Genome Atlas and GTEx project. miR-34a-5p, IMP3, and PD-L1 mRNA levels, IMP3 and PD-L1 protein levels were detected in breast cancer and adjacent normal tissues by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot. Correlations between miR-34a-5p and IMP3 and PD-L1 mRNAs were analyzed by Pearson’ s test. Immunohistochemistry was used to detect IMP3, PD-L1, and leukocyte differentiation antigen 44 variant 6 (CD44v6) expression in breast cancer and normal tissues, and the relationships between IMP3 and PD-L1 expression and clinicopathological parameters were analyzed. Target gene prediction and dual luciferase reporter assay were used to verify the targeted regulation of miR-34a-5p on IMP3 and PD-L1. MCF7 cells were divided into control group, miR-NC group, miR-34a-5p group, miR-NC+pcDNA-NC group, miR-NC+IMP3 group, miR-NC+PD-L1 group, miR-34a-5p+pcDNA-NC group, miR-34a-5p+IMP3 group, and miR-34a-5p+PD-L1 group. Cell proliferation, migration, and invasion were determined by MTT, colony-formation, scratch, and Transwell chamber tests, respectively. Expression levels of IMP3, PD-L1, CD44v6, matrix metalloproteinase-2 (MMP-2), MMP-9, and E-cadherin were detected by Western blot. Results 　The biological databases showed that higher expression levels of IMP3 and PD-L1 in breast cancer tissues were associated with shorter survival (P<0. 05). Expression levels of miR-34a-5p were significantly lower while expression levels of IMP3 and PD-L1 mRNAs and proteins were significantly higher in breast cancer tissues than in normal tissues. miR-34a-5p expression was negatively correlated with IMP3 and PD-L1 mRNAs, respectively (P<0. 05). Immunohistochemistry showed positive expression of IMP3, PD-L1, and CD44v6 in breast cancer, with higher IMP3 and PD-L1 expression associated with later TNM stage, lower degree of tumor differentiation, and increased risks of lymph node and distant metastases (P<0. 05). Dual luciferase assay verified the targeted regulation of miR-34a-5p on IMP3 and PD-L1. The cell viability, number of clones formed, scratch-healing rate, cell invasion, and expression levels of IMP3, PD-L1, CD44v6, MMP-2, and MMP-9 protein were all significantly lower and E-cadherin expression was significantly higher in the miR-34a-5p group compared with the control group and miR-NC group. The cell viability, number of clones formed, scratch-healing rate, cell invasion, and expression levels of IMP3, PD-L1, CD44v6, MMP-2, and MMP-9 proteins were all significantly increased while expression of E-cadherin protein was significantly decreased in the miR-NC+IMP3 and miR-NC+PD-L1 groups compared with the miR-NC+pcDNANC group. The cell viability, number of clones formed, rate of scratch healing, cell invasion, and expression levels of IMP3, PD-L1, CD44v6, MMP-2, and MMP-9 protein were all significantly increased while E-cadherin expression was significantly decreased in the miR-34a-5p+IMP3 and miR-34a-5p+PD-L1 groups compared with the miR-34a-5p+pcDNANC group (P< 0. 05). Conclusions 　miR-34a-5p can inhibit the proliferation, migration, invasion, and epithelialmesenchymal transition of breast cancer cells by targeting the expression of IMP3 and PD-L1.

Abstract: Objective　To investigate the effects of serum containing Fuzheng Kangai Decoction (FZKAD) on the proliferation, apoptosis, and cell cycle progression in human ovarian carcinoma HO-8910PM cells. Methods 　Forty Sprague-Dawley rats were divided randomly into control and low-dose (4. 725 g/ kg), medium-dose (9. 45 g/ kg), and high-dose (18. 9 g/ kg) FZKAD groups. After 7 days of intragastric administration, serum containing FZKAD was prepared and used for the culture of HO-8910PM cells. Cell proliferation was detected by MTT assay, colony-formation ability was detected by clone formation assay, apoptosis was detected by flow cytometry using Annexin V-fluorescein isothiocyanate/propidium iodide double-staining, cell cycle progression was detected by flow cytometry using propidium iodide single staining, and protein expression levels were detected by Western blot. Results　There was no significant difference in cell survival rates among the low-dose, medium-dose, and control groups after 24 h ( P>0. 05). However, cell survival rates in the other groups were significantly decreased after 24, 48 and 72 h (P<0. 05 or P<0. 01), and the colony-formation abilities were also significantly decreased in each dosage group (P<0. 01). Compared with the control group, the apoptosis rates and protein expression levels of P53 and Bax were significantly increased in the low-dose, medium-dose, and highdose groups (P<0. 05 or P<0. 01), while the protein expression level of Bcl-2 was decreased (P<0. 01). The percentage of cells in G₀ / G₁ stage was significantly increased in the low-dose, medium-dose, and high-dose groups compared with the control group (P<0. 05 or P<0. 01), while the percentages of cells in S and G₂ / M stages and protein expression levels of cyclin D1 and cyclin-dependent kinases 4 and 6 were decreased (P<0. 05 or P<0. 01). Conclusions　Serum containing FZKAD can inhibit the proliferation of human ovarian cancer HO-8910PM cells, related to the induction of apoptosis and cell cycle arrest.

Abstract: Objective　To observe expression of ferroptosis-related factors in an adenine-induced chronic kidney disease model, and investigate the mechanism of ferroptosis in the pathological process of chronic kidney disease. Methods Twenty rats were randomly divided into a control group (Con) and model group (CKD). The CKD model was established by 2. 5% adenine gavage. All rats were sacrificed after 6 weeks. Blood samples were collected to measure serum urea nitrogen (BUN) and serum creatinine (Scr). HE staining was performed to observe renal pathological changes. Masson staining was performed to observe interstitial fibrosis of renal tubules. Iron, malondialdehyde (MDA), and glutathione(GSH) concentrations were measured. Western blot was performed to detect the protein expression of iron ferroptosisrelated proteins including systemic Xc- subunit SLC7A11, peroxidase 4 (GPX4), and iron metabolism-related proteins including transferrin receptor 1 (TFR-1), ferritin heavy chain (FTH), ferritin light chain (FTL), and membrane iron transporter protein (FPN). Correlations between iron, MDA and GSH levels and interstitial renal fibrosis were analyzed. Results　Compared with the Con group, serum urea nitrogen and serum creatinine were significantly increased in the CKD group (P<0. 05). HE and Masson staining showed significant tubular dilatation and interstitial fibrosis. Iron and MDA concentrations were significantly increased (P<0. 05), and the GSH concentration was significantly decreased (P<0. 05). Immunohistochemistry showed that, 4-HNE protein expression was significantly increased and GPX4 protein expression was significantly decreased in the CKD group compared with the Con group. Western blot showed that SLC7A11, GPX4, TFR-1, and FPN protein expression was significantly decreased, while FTH and FTL expression was significantly increased compared with the Con group. Correlation analysis indicated that iron and MDA concentrations were positively correlated to the relative area (%) of renal fibrosis, and the GSH concentration was negatively correlated with them. Conclusions Ferroptosis is present in the adenine-induced CKD rat model and may be involved in renal fibrosis progression in CKD via the GSH-GPX4 axis.

Abstract: Objective 　To explore the effect of Rehmannia glutinosa polysaccharide (RGP) on apoptosis of osteoarthritis (OA) chondrocytes induced by sodium iodoacetate (MIA) via the regulation of long-chain non-coding RNA (lncRNA) maternal expression gene 3 (MEG3). Methods　Rat chondrocytes were cultured with MIA 0, 1, 2, 4, and 8 μmol/ L to induce chondrocyte injury, and were then treated with RGP 50, 100, 200, 400, and 800 mg/ mL, respectively, to detect the appropriate experimental concentration. Rats were divided into a normal group, MIA group, RGP group, RGP+control (NC) small interfering RNA (siRNA) group, and RGP+si-MEG3 group. Cell viability was detected by Cell Counting Kit-8 (CCK-8) assay and apoptosis was detected by Hoechst 33258 staining and flow cytometry. mRNA levels of MEG3, metalloproteinase 13 (MMP-13), type Ⅱ collagen-α1 (COL2A1), and proteoglycan (ACAN) were detected by real-time quantitative polymerase chain reaction. Protein levels of PI3K, phospho (p) PI3K, serine/ threonine kinase(AKT), p-AKT, BAX, BCL-2, and caspase3 were detected by Western blot. Results 　MIA decreased chondrocyte viability and induced apoptosis in a dose-dependent manner, decreased MEG3, COL2A1, and ACAN mRNA levels, and increased MMP-13 mRNA levels (P<0. 05). RGP 100, 200, 400, and 800 mg/ mL increased chondrocyte viability and MEG3 levels (P <0. 05). Cell viability, MEG3, COL2A1, and ACAN mRNA, and p-PI3K/ PI3K, p-AKT/ AKT, and BCL-2 protein levels were decreased in the MIA group compared with the control group, while the apoptosis rate, MMP-13 mRNA, and BAX and caspase3 protein levels were increased (P<0. 05). Cell viability, MEG3, COL2A1, and ACAN mRNA, and p-PI3K/ PI3K, P-AKT/ AKT, and BCL-2 protein levels were increased in the RGP group compared with the MIA group, while the apoptosis rate, MMP-13 mRNA, and BAX and caspase3 protein levels were decreased (P<0. 05). Knockdown of MEG3 weakened the protective effect of RGP on MIA-induced chondrocyte injury. Conclusions　RGP can promote the synthesis of chondrocyte extracellular matrix and inhibit cell apoptosis and MIA-induced chondrocyte damage, possibly acting via a mechanism related to the up-regulation of MEG3 expression and induction of PI3K/ AKT pathway activation.

Abstract: Objective　To investigate the therapeutic effect and mechanism of Gubi powder on osteoarthritis. Methods　New Zealand white rabbits were divided into a blank group, model group, positive group (diclofenac potassium gel), and Gubi powder group (n = 6 rabbits per group). A rabbit knee osteoarthritis model was constructed using the modified Hulth method, and the treatments were administered for 4 weeks after 8 weeks of modeling. Cartilage thickness was measured by toluidine blue staining and the Mankin score was derived after Muscovite O staining of cartilage tissue. Terminal deoxynucleotidyl transferase dUTP nick end labeling fluorescence staining was used to detect the apoptosis of chondrocytes in cartilage tissue. Collagen (Col) Ⅱ and collagen X protein expression levels in cartilage tissue were detected by immunohistochemistry and expression levels of Bax, cleaved-caspase-3, phospho (p) extracellular signalregulated kinase (ERK), p-p38, p-Smad2, p-Smad3, and transforming growth factor (TGF)-β1 in cartilage tissues were detected by Western blot. Results　Cartilage thickness was decreased, the Mankin score and chondrocyte apoptosis rate were increased, Col Ⅱ, p-Smad2, p-Smad3, and TGF-β1 protein expression levels were decreased, and Col X, Bax, cleaved-caspase-3, p-ERK, and p-p38 levels were increased in the model group compared with the control group. Cartilage thickness was increased, the Mankin score and chondrocyte apoptosis rate were decreased, Col Ⅱ, p-Smad2, p-Smad3, and TGF-β1 expression levels were increased, and Col X, Bax, cleaved-caspase-3, p-ERK, and p-p38 protein expression were decreased in the positive and Gubi powder groups compared with the model group. Conclusions 　Gubi powder showed good therapeutic efficacy against osteoarthritis in rabbits, by reducing chondrocyte apoptosis, stabilizing cartilage tissue structure, and promoting the regeneration and repair of cartilage tissue after injury. Its mechanism may be related to inhibition of the ERK/ P38 pathway and activation of the TGF-β/ Smad pathway.

Abstract: Objective　To explore the healing effect of xiaochaihu decoction in a rat model of chronic pyogenic osteomyelitis of the jaw. Methods　Sixty-five specific-pathogen-free rats were used to establish a model of chronic pyogenic osteomyelitis of the jaw, by introducing Staphylococcus aureus into round bone defects prepared using a bone drill. After 1 month, five rats were randomly selected to test the modeling result, and the other rats were divided randomly into four groups: group A, debridement+saline; group B, debridement+xiaochaihu decoction; group C, debridement+cefuroxime; and group D, debridement+xiaochaihu decoction+cefuroxime. Five rats in each group were sacrificed at 2, 4, and 8 weeks after administration. The extent of the bone defect was detected by cone beam computed tomography (CBCT), levels of the inflammatory cytokines interleukin (IL)-6 and IL-1β were detected by enzyme-linked immunosorbent assay, and bone morphogenetic protein-2 was detected by immunohistochemistry. Results　CBCT showed that the bone defects in groups B, C, and D had decreased at 2, 4, and 8 weeks after administration, compared with group A (P<0. 05). In addition, the bone defects were smaller in groups B and D compared with group C (P<0. 05), and smaller in group D compared with group B (P<0. 05). Levels of IL-6 and IL-1β were lower in groups B, C, and D compared with group A at 2, 4, and 8 weeks after administration, IL-1β levels were lower in groups B and D compared with group C, and levels of IL-6 were lower in group D compared with C (P<0. 05); however, there was no significant difference in IL-6 levels between groups B and C ( P>0. 05). IL-1β and IL-6 levels were both lower in group D compared with group B (P<0. 05). BMP-2 expression was detected in groups A, B, C, and D, with higher mean optical densities in groups B, C, and D compared with group A, higher optical densities in groups B and D compared with group C, and in group D compared with group B at 2, 4, and 8 weeks after administration (P< 0. 05). Conclusions 　We successfully established a rat model of chronic pyogenic osteomyelitis of the mandible using S. aureus. Xiaochaihu decoction improved chronic pyogenic osteomyelitis, and the therapeutic effect of xiaochaihu decoction combined with cefuroxime was better than that of either drug alone.

Abstract:Laboratory animal barrier contamination by pathogenic microorganisms during the operation of environmental facilities seriously affects research and animal health or leads to biosafety incidents, interference of experimental result, or interruption of experiments. However, elimination of contamination during their long-term operation is difficult ,and can occur due to careless management or operational details. Contamination by pathogenic microorganisms is a major problem for laboratory animal managers. After engaged in laboratory animal barrier facility management for many years, The author deeply felt the importance of details management to prevent infection by pathogenic microorganism. Therefore, summarized of the details problem combined facility layout with staff management based on years of working experience, which in order to be discussed and used for reference.

Abstract:Cachexia is a syndrome of multifactorial metabolic disorders involving multiple organs and is a common fatal factor in patients with malignant tumors. The major clinical symptoms are muscle atrophy and loss, and their mechanism is associated with excessive protein degradation and synthesis disorders. In recent years, traditional Chinese medicine has made a significant advantage in the use of few side effects, multi-targets, and multi-channel intervention diseases. It has unique value in preventing and treating tumor disease and muscle atrophy. This review mainly discusses the effect of muscle protein degradation and synthesis mediated by various signals on tumor Cachexia muscle atrophy and the regulatory role of traditional Chinese medicine to provide a reference for the clinical application and research of traditional Chinese medicine in the treatment of tumor Cachexia muscle atrophy.

Abstract:Vascular endothelial cells form a thin layer of flattened cells that cover the surface of the vessel wall, As an effector tissue, the vessel wall responds to various stimuli to release vasoactive substances to maintain homeostasis. However, endothelial cells are prone to dysfunction induced by multiple pathological factors, which is manifested by an impaired vasomotor function, thrombosis, and arterial wall proliferation. Studies have shown that vascular endothelial dysfunction is closely related to the occurrence and development of cardiovascular diseases such as atherosclerosis and heart failure. Therefore, effectively evaluating endothelial functions is essential to prevent and treat cardiovascular diseases. In this review, we discuss the functions and regulatory principles of the vascular endothelium and its relationship with cardiovascular diseases and summarize the basic principles and advantages and disadvantages of existing endothelial assessment techniques to assist in the diagnosis and treatment of cardiovascular diseases.

Abstract:Accumulating studies have shown that long non-coding RNA (lncRNA) plays major roles in endothelial injury, inflammation, cancer, and autoimmune diseases. Systemic sclerosis (SSc) is an autoimmune disease with an unclear pathogenesis. lncRNA may be involved in the occurrence and development of SSc by regulating immune disorders, microvascular disease, and fibrosis, and may be a biomarker of SSc to predict occurrence, activity and progression of the disease. Therefore, lncRNA may be a novel therapeutic target of SSc.

Abstract:Toxicity has become a major obstacle to the international use of traditional Chinese medicines, and a rational grading strategy for their toxicity is therefore needed. Although the existing traditional toxicity classification can help to guide the clinical use of traditional Chinese medicines, it lacks quantitative data and is not sufficiently accurate, with different sources reporting different toxicity classifications for the same drug. Modern research on toxicity classification mainly includes classification method based on LD50 of oral raw drugs, multi indicator comprehensive classification method, evaluation model of toxic traditional Chinese medicine based on “substance efficacy toxicity”, and the use of modern toxicology research models. Although these toxicity grading method achieve quantitative standards for traditional Chinese medicine toxicity grading, they deviate from the theoretical guidance of traditional Chinese medicine and differ significantly from clinical practice, failing to reflect the essence of clinical compound medication of traditional Chinese medicine. To sort previous studies on the toxicity of traditional Chinese medicines, this paper proposes a scoring and grading method based on data mining combined with toxicological studies. The proposed method is based on data mining of historical toxicity records for traditional Chinese medicines, clinical reports, and experimental in vitro and in vivo studies, as well as comprehensive modern toxicological research result, followed by the assignment of weighted scores to each item, to derive a toxicity classification method for traditional Chinese medicines. For example, aconite would be graded as highly toxic according to this procedure. This grading method has the advantages of focusing on clinical compound drug use, as well as providing guidance for clinical practice. It can quantitatively indicate the degree of toxicity, thus reflecting the modern characteristics of traditional Chinese medicine. This grading method needs further refinement, but after gradual improvement and refinement, this toxicity classification method for traditional Chinese medicines is expected to promote their rational clinical application and wider international use.