OBJECTIVE: To investigate the anti-ulcerative colitis mechanism of resveratrol through regulation of Wnt/β-catenin signaling pathway. METHODS: ①The experiment of ulcerative colitis induced by dextran sulfate sodium salt (DSS): 28 C57BL/6 mice were randomly divided into four groups including control group(n=7), DSS group(n=7), DSS+Resveratrol (DSS+Res) group(n=7) and Res group(n=7). The experiment lasted for 3 weeks. Ulcerative colitis of mice was induced by drinking DSS water and treated with resveratrol by intragastric administration. The mice were weighed daily and their activities and state of feces were recorded. After that, the mice were euthanized, the spleens were weighed, and the colonic length was measured.Hematoxylin-eosin staining (HE) was used to observe the pathological changes of the colon, and the expression of miR-31 in colonic tissue was detected by quantitative real-time PCR (qPCR). The expressions of β-catenin and Cyclin D1 were measured by Western blot. ②In vitro experiment: HCT 116 cells were treated with resveratrol at 10 mg/ml, the expressions of β-catenin, LDL receptor related protein-6 (LRP-6), frizzled-3 (FZD3) and c-Myc were detected. The expression of β-catenin was also detected in HCT 116 cells transfected with miRNA-31 mimic and miRNA-31 inhibitor. RESULTS: ① The body weight was decreased in DSS group, the activity was decreased and blood stool appeared. The colonic length of mice was shortened, the spleen was enlarged and the tissue was damaged seriously in DSS group. While the above symptoms were improved after resveratrol treatment. ② Resveratrol inhibited the expressions of miRNA-31, β-catenin and CyclinD1 in ulcerative colitis mice, and also down-regulated the expressions of β-catenin, LRP-6, FZD3 and c-Myc in HCT 116 cells. After transfection of miRNA-31 inhibitor, the expression of β-catenin was decreased in HCT 116 cells. CONCLUSION: Resveratrol suppresses DSS induced colitis by down-regulation of Wnt signal pathway. The down-regulation of Wnt signal may be related to miRNA-31.
OBJECTIVE: To investigate the anti-ulcerative colitis mechanism of resveratrol through regulation of Wnt/β-catenin signaling pathway. METHODS: ①The experiment of ulcerative colitis induced by dextran sulfate sodium salt (DSS): 28 C57BL/6 mice were randomly divided into four groups including control group(n=7), DSS group(n=7), DSS+Resveratrol (DSS+Res) group(n=7) and Res group(n=7). The experiment lasted for 3 weeks. Ulcerative colitis of mice was induced by drinking DSSwater and treated with resveratrol by intragastric administration. The mice were weighed daily and their activities and state of feces were recorded. After that, the mice were euthanized, the spleens were weighed, and the colonic length was measured.Hematoxylin-eosin staining (HE) was used to observe the pathological changes of the colon, and the expression of miR-31 in colonic tissue was detected by quantitative real-time PCR (qPCR). The expressions of β-catenin and Cyclin D1 were measured by Western blot. ②In vitro experiment: HCT 116 cells were treated with resveratrol at 10 mg/ml, the expressions of β-catenin, LDL receptor related protein-6 (LRP-6), frizzled-3 (FZD3) and c-Myc were detected. The expression of β-catenin was also detected in HCT 116 cells transfected with miRNA-31 mimic and miRNA-31 inhibitor. RESULTS: ① The body weight was decreased in DSS group, the activity was decreased and blood stool appeared. The colonic length of mice was shortened, the spleen was enlarged and the tissue was damaged seriously in DSS group. While the above symptoms were improved after resveratrol treatment. ② Resveratrol inhibited the expressions of miRNA-31, β-catenin and CyclinD1 in ulcerative colitismice, and also down-regulated the expressions of β-catenin, LRP-6, FZD3 and c-Myc in HCT 116 cells. After transfection of miRNA-31 inhibitor, the expression of β-catenin was decreased in HCT 116 cells. CONCLUSION:Resveratrol suppresses DSS induced colitis by down-regulation of Wnt signal pathway. The down-regulation of Wnt signal may be related to miRNA-31.