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[目的]观察雷公藤多苷片对右旋葡聚糖硫酸钠(DSS)诱导的小鼠溃疡性结肠炎(UC)模型结肠巨噬细胞自噬相关蛋白——自噬蛋白微管相关蛋白1轻链3(LC3)的表达变化,探讨其治疗UC的可能作用机制。[方法]SPF级雌性BALB/c小鼠随机分为4组:正常对照组、雷公藤多苷片混悬液灌胃组和美沙拉嗪片混悬液灌胃组和模型对照组。采用DSS复制BALB/c小鼠UC动物模型,随机分组后分别予美沙拉嗪片混悬液、雷公藤多苷片混悬液及蒸馏水灌胃给药28d后,取出结肠组织,分离培养结肠巨噬细胞,采用Western blot法检测自噬相关蛋白LC3II/I的表达。[结果]雷公藤多苷片混悬液灌胃组和美沙拉嗪片混悬液灌胃组较模型对照组自噬相关蛋白LC3II/I的表达明显下降。[结论]雷公藤多苷片能够通过抑制细胞自噬,抑制UC小鼠的炎症反应,对UC发病起到一定得保护作用。
[Objective] To observe the effect of tripterygium glycosides tablet on the expression of autophagy-related protein-autophagy protein microtubule-associated protein 1 in colonic macrophages induced by dextran sodium sulfate (DSS) in mouse ulcerative colitis (UC) Light chain 3 (LC3) expression changes to explore its possible mechanism of action of UC. [Methods] SPF female BALB / c mice were randomly divided into 4 groups: normal control group, tripterygium wilfordii suspension suspension group and mesalazine suspension group and model control group. The animal model of BALB / c mice was established by DSS. The rats were randomly divided into mesalazine suspension, tripterygium wilfordii suspension and distilled water for 28 days. The colon tissues were removed and the colon giant Western blot was used to detect the expression of autophagy-related protein LC3II / I. [Result] Compared with the model control group, the expression of autophagy-related protein LC3II / I in the intragastric administration group and the mesalazine suspension suspension group were significantly decreased. [Conclusion] Tripterygium glycosides tablet can inhibit the autophagy, inhibit the inflammatory reaction in UC mice and play a protective role in the pathogenesis of UC.