靛玉红对DSS诱导结肠炎小鼠紧密连接蛋白ZO-1表达的影响

Effects of indirubin on the expression of tight junction protein ZO-1 in DSS-induced colitis mice

目的探讨靛玉红治疗溃疡性结肠炎的作用机制。方法用硫酸葡聚糖钠(DSS)诱导实验性小鼠结肠炎模型,随机分为靛玉红高剂量组、靛玉红中剂量组、靛玉红低剂量组、美沙拉嗪组、模型I组、模型II组、正常组,每组各10只。其中模型I组于造模7天时处死,其余各组均在造模第7天开始灌胃给予相应的药物,每日1次,连续给药7天后处死;取小鼠结肠病变部位标本,检测结肠组织ZO-1蛋白表达及TNF-α、IFN-γ含量。结果模型I组结肠黏膜TNF-α、IFN-γ含量比正常组增加,ZO-1表达减少;与模型II组比较,靛玉红低、中、高剂量组和美沙拉嗪组TNF-α、IFN-γ含量明显减少,ZO-1表达明显增加,其中靛玉红高剂量组最为明显。结论靛玉红能够修复肠上皮损伤,通过降低TNF-α、IFN-γ含量,增加紧密连接蛋白ZO-1表达而发挥其改善肠上皮屏障功能、消除肠道炎症的作用。

Objective To study the mechanisms of indirubin in treating ulcerative colitis （UC）. Methods Ulcerative colitis was induced by dextran sulfate sodium （DSS） in. mice. The UC mice were randomly divided into indirubin high-dose group ,indirubin middle-dose group, indirubin low-dose group, 5-ASA group, model I group, model II group and normal group, 10 mice in each group. Mice in model I group were sacrificed on the 7th day. The other groups were given due treat- ments by garage from the 7th day, once a day for 7 days. After 7-day treatment, the mice＇ colon was sampled to detect the expression of ZO-1 protein, the contents of TNF-α and IFN-γ. Results Compared with the normal group, the expression of ZO-1 was significantly decreased and the contents of TNF-α and IFN-γ were markedly increased in model I group. Compared with the model iI group, the expression of ZO-1 was increased and the contents of TNF-α and IFN-γ were decreased in all treatment groups, especially in the indirubin high-dose group. Conclusion It is indicated that indirubin can repair the enteric epithelial barrier injury and eliminate intestinal inflammation by decreasing the contents of TNF-α and IFN-γ and increasing the expression of ZO-1.