慢性乙型肝炎肝脏微循环障碍发生发展机制的研究  

A study on the mechanism of intrahepatic microcirculation changes in patients with chronic hepatitis B and cirrhosis

作　　者：李志群[1] 张丰[1] 祝扬[1] 赵景民[2] 潘登[2] 杨建法[2] 赵雨来[2] 

机构地区：[1]北京市解放军第261医院,100094 [2]解放军第302医院病理科

出　　处：《实用肝脏病杂志》2010年第2期104-106,共3页Journal of Practical Hepatology

摘　　要：目的探讨慢性乙型肝炎患者肝脏微循环障碍的主要分子机制。方法选择不同纤维化分期CHB穿刺肝组织和肝硬化外科活检肝组织及健康肝移植供体肝组织,应用免疫组化EliVisionTM System法,检测肝组织中COX1、COX2、AngII、AT1及α-SMA蛋白表达情况,并分析它们与肝内小血管、微血管或肝窦病理改变的关系。结果在CHB肝组织内COX1、COX2、AngII、AT1、及α-SMA在血窦壁、肝内小的门静脉分支、肝动脉分支、中央静脉及小叶下静脉壁均呈不同程度的阳性表达,随肝纤维化程度的加重其表达水平明显升高,在活动期肝硬化肝组织内上述调节分子表达最强(x2=8.8535,P=0.0120)。结论肝纤维化和肝硬化程度与COX1、COX2等指标之间存在相关性。Objective To explore main molecular mechanism of introhepatic microcirculation obstruction induced by chronic hepatitis B virus.Methods The liver biopsy tissues from patients with chronic hepatitis B,cirrhosis and healthy control were obtained.α-smooth muscle actin（α-SMA）,cyclooxygenase2（COX2）,COX1,and angiotensinII in the fibrotic livers and cirrhosis were examined by using immunohistochemistry.Results α-SMA,COX2,COX1 and angiotensin II in hepatic sinusoidal wall,little portal venules branch,hepatic arteries branch,central vein,vein wall beneath lobules were positive.They were obviously up-regulated as compared to control.Conclusions Intrahepatic microcirculation changes was found in chronic hepatitis B and cirrhosis.

关 键 词：乙型肝炎 肝硬化 环氧合酶 血管紧张素 

分 类 号：R512.62[医药卫生—内科学]