细胞外信号调节蛋白激酶在新生鼠坏死性小肠结肠炎模型中的表达及意义

The Activation of Extracellular Signal-regulated Kinase on Neonatal Rat Model for Necrotizing Enterocolitis

目的观察新生大鼠坏死性小肠结肠炎(necrotizingenterocolitis,NEC)中细胞外信号调节激酶(extracellularsignal-regulatedkinase,ERK)的激化及胞内分布规律,探讨其在NEC发病机制中的作用。方法新生鼠随机分为不接受处理的正常对照组和NEC模型组(实验组),每组8只。于母鼠身边喂养3d,第4d处死。并取近回盲部肠组织1～2cm固定、包埋、切片、HE染色拍照,观察组织学变化及免疫组化观察ERK的表达,其它肠组织制备组织匀浆,取上清液检测肿瘤坏死因子(tumornecrosisfacror-α,TNF-α)和一氧化氮(nitricoxide,NO)的含量。结果实验组肠组织中ERK均发生活化并伴核转位(P<0.01),TNF-α、NO的含量明显升高(P<0.05)。结论ERK信号通路可能参与了NEC发病过程,并起着信号转导作用。

Objective To investigate the intracellular distribution and the avtivation of ERK on hypoxia-induced in neonatal rat NEC model and the role in the mechanism of NEC. Methods Newborn Wistar rats were divided randomly into experimental and control groups, 8 in each group. After NEC model, they were returned to their mothers .On the 4th day ,all the subjects were put to death. Intestinal tissue locates at the boundary of ileum and cecum were obtained to observe histological changes and ERK level by immunohistochemistry methods. Other intestinal tissue was turned to homo genate. After the homogenate was centrifuged, supernates were used to test the density of TNF-α and NO. Results In experimental group,activation of ERK with nuclear translocation was found （P 〈 0.01）,and the density of TNF-α and NO was significantly increased （ P 〈 0.05）. Conclusion ERK signal pathways might play important roles in the mechanism and signal transduction of NEC.