Xinhuang Tablets Improve Intestinal Barrier Function via Regulating Epithelial Tight Junctions in Dextran Sulfate Sodium-Induced Ulcerative Colitis Mice.

Abstract

Intestinal mucosal barrier dysfunction is involved in the pathogenesis of inflammatory bowel disease, including ulcerative colitis (UC). Xinhuang tablets (XHTs) have been prescribed for several kinds of inflammatory diseases, including UC, whereas its possible underlying molecular mechanisms had never been explored. Mouse model of UC was constructed by DSS treatment and followed by XHT treatment. Disease activity index, histopathological of colonic tissue, tumor necrosis factor-alpha (TNF-α), and serum amyloid A (SAA) levels in serum were further assessed. The underlying mechanism was further explored by determination of the expression of epithelial tight junction-related protein. XHT administration ameliorated dextran sulfate sodium (DSS)-induced clinical symptoms, colonic histological injury, and decreased the circulating levels of TNF-α and SAA. Moreover, XHT treatment significantly increased the protein levels of zona occludens (ZO)-1, whereas decreased the levels of phosphorylation of Elk-1. In conclusion, this study confirmed the therapeutic effects of XHT treatment on UC in a DSS-induced mouse model, and indicated that by increasing expression of epithelial tight junctions and decreasing phosphorylation of Elk-1 might be one of the underlying mechanisms of XHT treatment on UC.