Effect of Curcumin on Expression of Differentiation-related Factors in Th17 in Mice with Ulcerative Colitis

OBJECTIVE To observe the effect of curcumin on the expression of differentiation-related factors of T helper cell 17 (Th17) in mice with ulcerative colitis, exploring the potential mechanism of curcumin in the treatment of ulcerative colitis(UC). METHODS Fifty SPF grade BALB/c mice were randomly divided into five groups:blank control group, model group, curcumin low-dose group, curcumin high-dose group and sulfasalazine control group, 10 mice in each group. UC model was established by dextran sulphate sodium(DSS), then daily by means of intragastric administration for 7 d. During the course of experiment, the clinical symptoms of mice were recorded, and the disease activity index (DAI) score was recorded. At the end of the experiment, the mice were sacrificed, and the colon macroscopic damage index (CMDI) was scored. The pathological changes of colon tissue were observed under microscope and the tissue damage index (TDI) was evaluated. The expression levels of IL-6, IL-17 and TGF-b in colon tissues of mice were detected by ELISA. And the expression levels of retinoid-related orphan receptors gt (RORgt) and phosphorylated STAT3 (p-STAT3) in colon tissues of mice were detected by Western blotting. RESULTS Compared with the normal control group, the scores of DAI, CMDI and TDI in model group increased significantly(P<0.01), the expression level of TGF-β decreased significantly(P<0.01), the expression levels of IL-6, IL-17, RORγt, STAT3, p-STAT3 increased significantly(P<0.01). Compared with the model group, the scores of DAI, CMDI and TDI in curcumin treatment group decreased significantly(P<0.05 or P<0.01), the expression level of TGF-β increased significantly(P<0.05 or P<0.01), the expression levels of IL-6, IL-17, RORγt, STAT3, p-STAT3 decreased significantly(P<0.05 or P<0.01). CONCLUSION Curcumin can improve the clinical symptoms of UC mice and alleviate the damage of colon tissue. The mechanism of curcumin in treating UC may be related to regulating the differentiation function of Th17 cells.