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.

目的 本研究基于小鼠葡聚糖硫酸钠（dextran sulfate sodium, DSS）诱导的结肠炎模型，探讨白术多糖（Atractylodis Rhizoma Polysaccharide）通过调控Th17/Treg平衡改善结肠炎的作用机制。方法 采用DSS诱导构建小鼠结肠炎模型，以白术多糖对小鼠进行干预治疗。检测各组小鼠的疾病活动指数（disease activity index, DAI）；采用苏木精-伊红（HE）染色法分析结肠组织病理变化；通过免疫组织化学与蛋白质印迹（Western Blot）技术检测小鼠结肠组织中STAT相关蛋白及紧密连接关键蛋白的表达水平；采用流式细胞术分析肠系膜淋巴结淋巴细胞的Th17与Treg细胞分化能力。结果 DSS模型组小鼠体重显著下降，DAI显著升高。经白术多糖干预后，小鼠体重显著回升，DAI指数降低。HE染色结果显示，DSS模型组小鼠结肠黏膜出现严重病理损伤，而白术多糖干预可有效缓解黏膜损伤。免疫组织化学与蛋白质印迹结果显示，白术多糖治疗后小鼠结肠组织中闭合蛋白（Occludin）与紧密连接蛋白ZO-1的表达水平显著上调（P<0.01）。流式细胞术结果显示，白术多糖干预后，肠系膜淋巴结中Th17细胞比例显著下调，而Treg细胞比例显著升高。结论 白术多糖可通过改善Th17/Treg细胞失衡，显著缓解DSS诱导的结肠炎小鼠的炎症状态。