目的:观察溃结灵对溃疡性结肠炎(UC)大鼠结肠粘膜IKK-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,大鼠随机分为六组:正常对照组、模型对照组、溃结灵低、中、高剂量组、SASP阳性对照组。治疗10 d后处死大鼠取结肠组织,采取免疫组化(IHC)法检测IKK-α的阳性细胞表达率。结果:模型组结肠粘膜IKK-α蛋白阳性细胞表达率明显高于正常对照组(P〈0.01),溃结灵中剂量组结肠粘膜IKK-α蛋白阳性细胞表达率明显低于模型组(P〈0.05),溃结灵高剂量组和SASP阳性对照组结肠粘膜IKK-α蛋白阳性细胞表达率明显低于模型组(P〈0.01)。结论:溃结灵使TNBS法UC大鼠模型结肠粘膜IKK-α蛋白阳性细胞表达率明显降低,这可能是其治疗UC作用的机理之一。
Objective:To explore the changes of protein expression of IKK-α as well as the effects of Kuijieling Decoction(KD) on colonic mucosa of ulcerative colitis(UC) model rats.Methods:UC model rats were induced by TNBS.The rats were randomly divided into six groups:normal control(NC) group,model control(MC) group,Kuijieling low dose(KLD),middle dose(KMD) group,high dose(KHD) group and SASP group.After 10-days′ treatment the rats were killed to get their colonic tissues.The positive rate of IKK-α expression was detected by immunohistochemical(IHC).Results:The positive rate of IKKα in MC group was significantly higher than that in NC group(P〈0.01).The positive rate of IKK-α in KMD group was significantly lower than that in MC group (P〈0.05).The positive rate of IKK-α in KHD and SASP group were significantly lower than that in MC group(P〈0.01).Conclusion:IKK-α may be involved in the pathogenesis of UC,and KD can inhibit positive rate of IKK-α in colonic mucosa of UC model rats induced by TNBS.The inhibitory effects of KD on UC may be associated with this.