溃结灵对溃疡性结肠炎大鼠结肠黏膜IκB-α蛋白表达的作用

目的:观察溃结灵对溃疡性结肠炎(UC)大鼠结肠黏膜核转录因子-κB(NF-κB)的抑制蛋白(IκB)-α蛋白表达的作用,对其作用机制进行初步探讨。方法:采用三硝基苯磺酸(TNBS)法制作UC大鼠模型,大鼠随机分为以下6组:正常对照组、模型对照组、溃结灵低剂量组、中剂量组、高剂量组、阳性药柳氮磺胺吡啶(SASP)组。治疗10天后处死大鼠取结肠组织,采取免疫组化(IHC)法检测IκB-α的阳性细胞表达率。结果:模型组结肠黏膜IκB-α蛋白阳性细胞表达率明显高于正常对照组(P<0.01);溃结灵高剂量组结肠黏膜IκB-α蛋白阳性细胞表达率明显低于模型组(P<0.05)。结论:溃结灵使TNBS法UC大鼠模型结肠黏膜IκB-α蛋白阳性细胞率明显降低,这可能是其治疗UC作用的机理之一。

Effect of Kuifieling Decoction on Proteins Expression of IκB -α in Colonic Mucosa of Ulcerative Colitis Model Rats

Objective: To explore the changes of protein expression of IκB-α as well as the effects of Kuijieling Decoction(KD)in colonic mucosa of ulcerative colitis(UC)model rats.Methods: UC model rats were induced by TNBS.The rats were randomly divided into six groups as follows: normal control(NC) group,model control(MC) group,Kuijieling low dose(KLD) group,Kuijieling medium dose(KMD) group,Kuijieling high dose(KHD) group and SASP group.After 10-days treatment the rats were killed to get their colonic tissue.Detect positive rate of IκB-α expression by immunohistochemical(IHC).Results:The positive rate of IκB-α in MC group was significantly higher than that in NC group(P<0.01).The positive rate of IκB-αin KHD group was significantly lower than that in MC group(P<0.05).Conclusion: IκB-α may be involved in the pathogenesis of UC,and KD could inhibit positive rate of IκB-α in colonic mucosa of UC model rats induced by TNBS.The inhibitory effects of KD on UC might be associated with the inhibition of positive rate of IκB-α.