肝性脑病发病机制中氨中毒假说的研究进展  

The Research Progress of Ammonia Poisoning Hypothesis in the Pathogenesis of Hepatic Encephalopathy

作　　者：陈敏[1] 陈维顺[1] 

机构地区：[1]中南大学湘雅医学院株洲临床学院株洲市中心医院消化内科

出　　处：《医学综述》2016年第3期483-486,共4页Medical Recapitulate

摘　　要：肝性脑病(HE)是严重肝病患者的常见并发症和死亡原因之一。其发病机制的研究对于HE的早期诊断和治疗及其预防具有重大的意义。近年来,针对HE发病机制的研究已有很多,氨中毒假说仍处于核心地位。氨对星形胶质细胞结构、代谢及功能的影响是HE的病理生理基础,炎症反应、细胞的氧化及硝基化、肠内微生态的改变及神经类固醇等可能与氨协同作用,共同促进HE的发生。Hepatic encephalopathy （HE） is a neumpsychiatric complication of severe liver disease and has been a common cause of death for affected patients. Research about the mechanism of HE plays an impor- tant role in the treatment and prevention of HE. In recent years, there are plenty of studies of the pathogenesis of hepatic encephalopathy, among which the central role of ammonia poisoning remains incontrovertible. Ammonia＇s impact on the structure, metabolism and function of astrocytes is the pathophysiological basis of HE. Inflammation, oxidative stress and nitrocellulose, the change of intestinal microecology possibly act synergistically with ammonia to promote the occurrence of HE.

关 键 词：肝性脑病 氨中毒假说 发病机制 星形胶质细胞 

分 类 号：R575[医药卫生—消化系统]