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.

中文翻译：

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新黄片通过调节葡聚糖硫酸钠诱导的溃疡性结肠炎小鼠的上皮紧密连接来改善肠屏障功能。

肠粘膜屏障功能障碍与炎症性肠病（包括溃疡性结肠炎（UC））的发病机理有关。新黄片（XHTs）已被指定用于包括UC在内的多种炎症性疾病，而其潜在的潜在分子机制从未被探索过。通过DSS处理并随后进行XHT处理来构建UC的小鼠模型。进一步评估疾病活动指数，结肠组织的病理组织学，肿瘤坏死因子-α（TNF-α）和血清中的淀粉样蛋白A（SAA）水平。通过确定上皮紧密连接相关蛋白的表达来进一步探索其潜在机制。XHT给药可改善硫酸右旋糖酐钠（DSS）引起的临床症状，结肠组织学损伤，并降低TNF-α和SAA的循环水平。此外，XHT处理显着增加了Zona咬合蛋白（ZO）-1的蛋白质水平，而降低了Elk-1的磷酸化水平。总之，这项研究证实了XHT治疗对DSS诱导的小鼠模型中UC的治疗作用，并表明通过增加上皮紧密连接的表达并降低Elk-1的磷酸化可能是XHT治疗糖尿病的潜在机制之一。 UC。