血管内皮细胞在门静脉高压性结肠病形成中的作用

The role of vascular endothelial cells in the pathogenesis of portal hypertensive colopathy(PHC)

目的探讨血管内皮细胞在门静脉高压性结肠病(PHC)形成中的作用。方法成年雄性Wistar大鼠19只,随机抽取8只作为正常组,其余大鼠按复合因素法制作肝硬化模型,10周后门静脉取血测定一氧化氮(NO)、肿瘤坏死因子(TNF)-α含量,取大鼠降结肠全层行免疫组织化学染色,观测黏膜下层血管内皮细胞,测定一氧化氮合酶(NOS)、TNF-α表达量。另取结肠组织行电镜观察。结果电镜下观察模型组可见内皮细胞分泌小泡增多,肌微丝形成。诱导型NOS(iNOS)、TNF-α在血管内皮细胞高度表达,与正常组相比差异有统计学意义(P<0.05)。血清NO、TNF-α显著增高,与正常组相比差异具有统计学意义(P<0.05)。结论肝硬化时,血管内皮细胞成为生成NO、TNF-α的主要细胞,这些炎症因子直接参与了PHC的形成。

Objective To explore the role of vascular endothelial cells in the pathogenesis of portal hypertensive colopathy （PHC）. Methods Adult male wistar rats were randomly divided into the control group （ n = 8） and the model group （71 ：： 11 ）. The 11 rats were made portal hypertension （PHT） by composite factors methods. Ten weeks later, the nitricoxide synthase and tumor necrosis factor were observed by immunohistochemical staining and then analyzed by image analysis system. After conventional handling, submueosal vascular endothelial cells were observed by transmission electron microscope. The level of NO and TNF-α in blood serum were detected. Results The expression of iNOS and TNF-α in submucosal vascular endothelial cells in model group was significantly higher （P 〈 0.05）, the level of NO and TNF-α in model group was significantly higher than that in normal control group （P〈0.05）. Conclusion Vascular endothelial cells mainly generate NO and TNF-α in cirrhotic rats.