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缺氧诱导因子1-α在酒精性肝病形成中的表达
引用本文:陈韶华,虞朝辉,厉有名. 缺氧诱导因子1-α在酒精性肝病形成中的表达[J]. 中华肝脏病杂志, 2004, 12(7): 417-419
作者姓名:陈韶华  虞朝辉  厉有名
作者单位:310003,杭州,浙江大学医学院附属第一医院消化内科
摘    要:目的 研究缺氧诱导因子1-α(HIF1-α)在洒精性肝病动物模型的表达情况,探讨其与酒精性肝病的关系。方法 采用酒精灌胃法建立酒精性肝病动物模型,应用逆转录聚合酶链反应(RT-PCR)法和免疫组织化学染色法检测大鼠肝组织HIF1-α mRNA和蛋白水平。结果 RT-PCR结果显示模型组大鼠HIF1-α mRNA表达阳性率为62.5%(5/8),对照组为16.7%(2/12),x~2=3.94,P<0.05。两组大鼠肝脏HIF1-α多克隆抗体免疫组织化学染色评分分别为3.13±0.83和0.83±1.27,差异有非常显著必,t=4.88,P<0.01。结论 HIF1-α在酒精性肝病动物模型的表达明显增高,缺氧是酒精性肝病的发病机制之一。

关 键 词:缺氧诱导因子1-α 酒精性肝病 动物模型 检测 发病机制
修稿时间:2003-07-04

Hypoxia inducible factor 1-α mRNA expression in alcoholic liver disease
CHEN Shao-hua,YU Chao-hui,LI You-ming. Digestive Department,the First Affiliated Hospital,Zhejiang University,Hangzhou ,China. Hypoxia inducible factor 1-α mRNA expression in alcoholic liver disease[J]. Chinese journal of hepatology, 2004, 12(7): 417-419
Authors:CHEN Shao-hua  YU Chao-hui  LI You-ming. Digestive Department  the First Affiliated Hospital  Zhejiang University  Hangzhou   China
Affiliation:Digestive Department, the First Affiliated Hospital, Zhejiang University, Hangzhou 310003, China.
Abstract:OBJECTIVE: To investigate the effect of hypoxia on chronic alcoholic liver disease. METHODS: Twenty four male Sprague-Dawley rats were randomly into two groups. The alcohol group (n=12) was fed 56% (v/v) of ethanol once per day by gastric infusion at 8 g/kg body weight for 24 weeks. The control group (n=12) was gastrically infused with normal saline with the same dose. At the end of 24 weeks, a blood sample was collected for determination of hepatic enzymes and then the rat was killed. Liver specimens were obtained for immunohistochemical staining and frozen at -80 degrees C used for RT-PCR. RESULTS: Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity increased significantly compared to the control group. A significant elevation in the expression of HIF1-alpha in liver of alcohol group was found compared to the control group. CONCLUSION: Hypoxia inducible factor 1-alpha expression was activated by ethanol-induced injury. This information suggested that hypoxia was involved in mechanism of alcoholic liver disease.
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