Toll样受体4、核转录因子-κB p65在小鼠溃疡性结肠炎中的表达及意义

The significance of TLR4 and NF-κB p65 expression in the ulcerative colitis

目的探索Toll样受体4(TLR4)和核转录因子-κB(NF-κB)在小鼠溃疡性结肠炎(UC)中的表达及意义,从而探讨该信号通路在UC发病机制中可能的作用。方法将20只雄性Balb/c小鼠随机分为正常组(N组)和模型组(M组),每组各10只。采用葡聚糖硫酸钠诱导UC模型,各组于造模后7 d取病变处结肠组织,进行组织学评分,HE染色观察大体形态、组织学评分和免疫组化染色观察NF-κB和TLR4的表达情况。结果 TLR4和NF-κB在M组小鼠结肠黏膜表达显著高于N组(P<0.05);且TLR4与NF-κB的表达呈正相关,Pearson相关系数r为0.816。结论TLR4和NF-κB的高表达提示该信号传导通路激活导致下游炎症因子的释放可能是UC发生的机制之一。

Objective To explore the might mechanism that through the significance of TLR4 and NF-κB p65 expression in the ulcerative colitis.Methods 20 Balb/c mice were randomly divided into normal group（group N） and UC model group（group M）,with 10 mice in each group.Using the DSS to induce UC model,the colonic tissue were collected at 7 d in each group,and the expression of TLR4,NF-KB and pathological change were tested with immunohistochemistry and HE staining methods and histopathological score.Results The expression of TLR4 and NF-κB in M group was higher than that of group N（P 0.05）,and the expression of TLR4 was parallel with that of NF-kB.Pearson correlation coefficient r was 0.816.Conclusion The inflammtory response following TLR4/NF-κB signaling pathway activated plays a role in the mechanism of UC.