中文摘要：

目的以核因子-κB（nuclear facter-κB,NF-κB）p65反义寡核苷酸（ASODN）及西药柳氮磺胺吡啶（SASP）为对照,观察清肠化湿方对三硝基苯磺酸（TNBS）法诱导小鼠溃疡性结肠炎（UC）模型结肠黏膜天冬氨酸特异酶切的半胱氨酸蛋白酶-3（Caspase-3）、闭锁小带蛋白-1（ZO-1）表达的影响。方法采用TNBS诱导小鼠UC模型,并随机分为清肠化湿方组、SASP组、清肠化湿方＋SASP组、ASODN组、模型对照组、空白对照组,治疗7 d后处死小鼠,取小鼠结肠标本,采用HE染色法观察各组小鼠结肠病理形态,并采用Western blot法检测各组小鼠结肠上皮细胞Caspase-3及ZO-1蛋白表达水平。结果模型对照组小鼠Caspase-3蛋白表达明显高于空白对照组（P〈0.05）;清肠化湿方组Caspase-3蛋白表达低于模型对照组（P〈0.05）,与空白对照组比较差异无统计学意义（P〉0.05）。模型对照组小鼠ZO-1蛋白表达明显低于空白对照组（P〈0.05）;清肠化湿方组ZO-1蛋白表达高于模型对照组（P〈0.05）,与空白对照组比较差异无统计学意义（P〉0.05）。结论清肠化湿方对UC模型小鼠具有治疗作用,其抑制肠上皮细胞Caspase-3蛋白表达、增强ZO-1的表达,抑制肠黏膜组织细胞凋亡,恢复正常的肠黏膜屏障形态和功能可能是其作用机制的一部分。

英文摘要：

Objective To take NF- κB p65 ASODN and the western medicine SASP as the controls to observe the impacts of Qingchang Huashi Formula on the expressions of Caspase- 3 and ZO- 1 in ulcerative colitis（ UC） models of mice induced by TNBS methods. Methods TNBS method was adopted to induce UC models,which were randomized into a Qingchang Huashi Formula group（ Formula group）,a SASP group, Formula ＋ SASP group,ASODN group,a model control group and a blank control group. The mice were sacrificed in 7 days of treatment and the colon samples were collected. HE method was used to observe the pathologic morphology of colons in the experimental mice in each group. Western Blot method was applied to determine the expressions of Caspase- 3 and ZO- 1 in each group. Results Capspase- 3 expression in the model control group was higher apparently than that in the blank control group（ P〈0. 05）,Capsase- 3 expression in the Formula group was lower than that in the model control group（ P〈0. 05）,but had no statistical difference as compared with the blank control group（ P〈0. 05）. ZO- 1 expression in the model control group was lower apparently than that in the blank control group（ P〈0. 05）,that in the Formula group was higher than that in the model control group（ P〉. 05）,but had no statistical difference as compared with the blank control group（ P〈0. 05）. Conclusion Qingchang Huashi Formula had the therapeutic effect on UC models of mice. It suppresses epithelial cell Caspase- 3 expression and intensifies ZO- 1 expression,inhibits intestinal mucosal apoptosis and recovers the normal morphology and function of intestinal mucosal barrier. All of those could be the effect mechanism of the formula.