Atractylodis Rhizoma Polysaccharide ameliorates dextran sulfate sodium-induced colitis by regulating Th17/Treg balance

Objective To explore the mechanism of the action of Atractylodis Rhizoma Polysaccharide on regulating Th17/Treg balance to ameliorate colitis based on the dextran sulfate sodium (DSS)-induced colitis model in mice.Methods Based on the DSS-induced mouse colitis model, we administered Atractylodis Rhizoma Polysaccharide to mice for intervention treatment. The disease activity index (DAI) of mice in each group was analyzed. The pathological changes of colon tissue were analyzed by the HE staining method. The expression of STAT-related proteins and tight junction key proteins in mouse colon tissues was analyzed by immunohistochemistry and Western Blot. The differentiation ability of Th17 and Treg cells of lymphocytes in mesenteric lymph nodes was analyzed by flow cytometry.Results The mice in the DSS group showed a significant decrease in body weight and a significant increase in DAI. After the intervention of Atractylodis Rhizoma Polysaccharide, the weight of mice increased significantly and the DAI index decreased. H&E staining results showed that the colonic mucosa of mice in the DSS group showed severe pathological damage, while the intervention of Atractylodis Rhizoma Polysaccharide effectively alleviated the mucosal damage. The results of immunohistochemistry and Western blot showed that the expression of Occludin and ZO-1 proteins was significantly increased (P<0.01) in the mice after treatment with Atractylodis Rhizoma Polysaccharide. Occludin and ZO-1 protein expression in mice treated with Atractylodis Rhizoma Polysaccharide were significantly increased (P<0.01). Flow cytometry results showed that the proportion of Th17 cells in mesenteric lymph nodes was significantly down-regulated, while the proportion of Treg cells was significantly increased after the intervention of Atractylodis Rhizoma Polysaccharide.Conclusion Atractylodis Rhizoma Polysaccharide can significantly attenuate the inflammatory condition of DSS-induced colitis mice by improving the Th17/Treg imbalance.