中文摘要：

目的 观察清肠化湿方对三硝基苯磺酸（TNBS）诱导的溃疡性结肠炎小鼠肠道Th17/Treg平衡的调节作用,以探讨其治疗溃疡性结肠炎（UC）的可能机制.方法 使用TNBS造模成功后,分为空白组、模型组、清肠化湿方组（12.8 kg/d）、柳氮磺胺吡啶（SASP）组（0.5 kg/d）.一次性ig给药,连续7d后处死小鼠;免疫组化法观察结肠组织中IL-17、Foxp3的浸润情况,Western blot法检测结肠组织RORγt和Foxp3蛋白的表达水平.结果 清肠化湿方组小鼠结肠组织中IL-17表达低于模型组（P＜0.05）;RORγt蛋白表达较模型组明显降低（P＜0.01）,且与SASP组比较差异有统计学意义（P＜0.05）;Foxp3蛋白表达较模型组升高（P＜0.05）.结论 清肠化湿方可能通过下调RORγt表达抑制Th17细胞分化、IL-17产生,通过上调Foxp3表达促进Treg细胞形成,从而调节溃疡性结肠炎小鼠Th17/Treg平衡,抑制肠道炎症.

英文摘要：

OBJECTIVE To observe possible mechanism of the Qingchang Huashi Fang＇s therapeutic effect on Ulcerative Colitis （UC） through regulating Th17/Treg on trinitrobenzene sulfonic acid induced colitis in mice.METHODS Mice successfully modeled with TNBS were divided into blank model,Qingchang Huashi Fang （12.8 crude drug kg/d） and SASP （0.5 g/kg） groups.All Mice,single administration for 7 days,were executed to collect colon tissues and cut out for related inspections.The expression of IL7 and Foxp3 in colonic epithelium was checked up with immunohistochemical method,and measure RORγt and Foxp3 protein in colonic epitheliumand by western blotting method.RESULTS The expression of IL7 in colonic tissues of Qingchang Huashi Fang group were lower than those in blank model group （P＜0.05）,and the expression of RORγt protein was significantly lower than those in blank model group （P ＜ 0.01）.Foxp3 protein was higher than those in model group （P＜0.05）.CONCLUSION Qingchang Huashi Fang can inhibit Th17 cell differentiation and IL7 generation through lower down egulation RORγt.It can promote Treg cell expression through regulation Foxp3.Qingchang Huashi Fang can effectively inhibit inflammation in TNBS induced colitis in mice through regulation Th17 Treg balance.