OBJECTIVE To investigate the protective effects of nitidine chloride (NC) on dextran sodium sulfate (DSS) - induced ulcerative colitis (UC) in mice by targeting miR-31 and its underlying mechanisms. METHODS DSS at the concentration of 1% was used to induce UC in mice. Thirty C57BL/6 male mice were randomly divided into four groups normal control group (n=7), DSS group (n=8), DSS + NC group (7.27 mg/kg) (n=8) and NC group (n=7). DSS was added in drinking water, and NC was administrated by gavage. The period of modeling lasted for 3 weeks. The control group and NC group drank sterile water every day, DSS group and DSS + NC group drank 1% DSS water in the first week, normal water in the second week and 1% DSS water in the third week. In the last week of modeling, mice in control group and DSS group were given 0.5% CMC-Na by gavage, while mice in DSS + NC group and NC group were given NC by gavage.  https://www.selleckchem.com/products/GDC-0980-RG7422.html  After the establishment of the model, the disease activity index (DAI) related to colitis was observed, the pathological score of colon tissue was evaluated by HE staining, the expression level of miR-31 in colon tissue was detected by qPCR, and the protein expressions of NF -κ B and COX-2 in colon tissue were detected by Western blot. RESULTS ① Compared with DSS group, the DAI in the DSS + NC group was decreased (P＜0.01). The colonic pathological injury was obviously ameliorated after treated by NC. ② Compared with normal control group, the expression of miR-31 in colonic tissue of DSS group was increased significantly(P＜0.01), compared with DSS group, the expression of miR-31 was decreased after treatment with NC(P＜ 0.05). ③ Compared with DSS group, the levels of inflammatory protein NF-κB and COX-2 in DSS + NC group was decreased significantly (P＜0.05). CONCLUSION Nitidine chloride has obvious therapeutic effects on DSS induced mouse colitis, and its anti-inflammatory mechanism is related to the down-regulation of miR-31 expression.OBJECTIVE To study the mechanisms of curcumin alleviating oxidative stress and spleen apoptosis induced by overtraining in rats by regulating Kelch-like ECH-associated protein-1 (Keap1)-nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) signaling pathway. METHODS Male Wistar rats of 7 weeks old were divided into control group (C group, 12), overtraining group (OM group, 11), curcumin + overtraining group (COM group, 14). The C Group did not undergo any exercise intervention. The OM and COM group underwent 8-week incremental load swimming training. During the training, rats in the COM group were treated with curcumin at the dose of 200 mg/(kg·d) in the volume of 5 ml/kg by gavage, and rats in the other groups were given an equal volume of solvent, 0.5% sodium carboxymethylcellulose. Twenty-four hours after the last training, the spleen index was calculated by weighing, the pathological changes of the spleen were observed by light microscopy, and the biochemical indicators of ions of Bcl-2, Nrf2 and HO-1 in spleen were increased (P＜0.05 or P＜0.01); serum Cor level, spleen apoptosis level, MDA concentration and the expression of Bax were decreased (P＜0.05 or P＜0.01). The change trend of T/Cor ratio between groups was consistent with the change of testosterone, and the change trend of Bcl-2/Bax ratio was consistent with the change of Bcl-2. CONCLUSION The 8-week incremental load excessive swimming training aggravated spleen apoptosis, led to pathological changes and dysfunction of spleen. Curcumin can up-regulate expression of Nrf2 and HO-1, alleviate oxidative stress induced by overtraining, enhance Bcl-2 expression and attenuate Bax expression, thereby inhibiting excessive spleen apoptosis of rats, protecting the structure and function of spleen.OBJECTIVE To investigated the effects of dihydromyricetin on cognitive and affective disorders induced by chronic social defeat stress and its possible mechanism in mice. METHODS C57BL/6J mice were randomly divided into control group (Control), chronic social defeat stress group (CSDS) and chronic social defeat stress + DHM group (CSDS+DHM) (14 mice in each group). The mice received chronic social defeat stress and were injected with DHM or vehicle intraperitoneally. A part of mice were subjected to (10 mice of each group) novel object recognition test (NOR), Y maze test, open field test (OFT), social interaction test (SIT), forced swimming test (FST) and tail suspension test (TST). The other mice (4 mice of each group) were decapitated and the expression levels of SIRT1 in hippocampus were detected by Western blot. RESULTS Compared with the control group, the learning and memory of the CSDS group were reduced significantly, the anxiety level was increased significantly, the immobility time in TST and FST was increased significantly, and the SIRT1 protein level in hippocampus was reduced significantly (P＜ 0.05 or P＜ 0.01); Compared with the CSDS group, the learning and memory of the CSDS + DHM group were improved significantly, the anxiety level of the mice was reduced significantly, and the immobility time in TST and FST was reduced significantly. The protein level of SIRT1 in hippocampus was increased significantly (P＜ 0.05 or P＜ 0.01). CONCLUSION DHM ameliorates the cognitive impairment, anxiety like behavior and depression like behavior of mice induced by CSDS and up-regulates the expression of SIRT1 protein.OBJECTIVE To observe the effects of the neurogenesis in the dentate gyrus (DG) of the hippocampus on depression-like behaviors in adult Wistar Kyoto (WKY) rats. METHODS There were three groups in total (n = 10) ① the control (Wistar) group 9-week-old Wistar rats were treated with saline for 3 weeks (10 mg/kg, intragastric administration); ② the depression model (WKY) group WKY rats of the same age, tested for depression-like behaviors, were as a rat model of depression, and were treated with saline for 3 weeks (10 mg/kg, intragastric administration); ③ the positive control (AMI+WKY) group WKY rats of the same age were treated with amitriptyline for 3 weeks (10 mg/kg, intragastric administration). The neurogenesis in hippocampus was detected by immunofluorescence staining for Ki67 (a neuronal proliferation marker) and DCX (an immature neuronal marker). The depression-like behaviors were assessed by sucrose preference test (SPT), open field test (OFT) and forced swimming test (FST). RESULTS ① When compared with Wistar rats, the number of Ki67+ cells and DCX+ cells of the DG in WKY rats were decreased by 33.