《中国康复理论与实践》

《中国康复理论与实践》 ›› 2010, Vol. 16 ›› Issue (2): 136-139.

• 论文 • 上一篇    下一篇

氨在肝性脑病发病机制中的作用

张清俊，刘雁勇，刘赫，左萍萍   

  1. 中国医学科学院基础医学研究所，北京协和医学院基础学院药理系，北京市100005。
  • 收稿日期:2009-12-01 修回日期:1900-01-01 出版日期:2010-02-25 发布日期:2010-02-25
  • 通讯作者: 左萍萍

Role of Ammonia in the Pathogenesis of Hepatic Encephalopathy (review)

ZHANG Qing-jun, LIU Yan-yong, LIU He, et al.   

  1. Department of Pharmacology, School of Basic Medicine, Peking Union Medical College & Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing 100005, China
  • Received:2009-12-01 Revised:1900-01-01 Published:2010-02-25 Online:2010-02-25

PDF (PC)

被引次数

39

摘要： 氨中毒学说是肝性脑病机制的经典学说之一。本文从氨中毒的角度，对氨引起的神经系统能量代谢、氧化应激、线粒体通透性转换(MPT)、GABA和谷氨酸(Glu)能神经递质系统、细胞内信号转导、水通道蛋白4(AQP4)表达的改变以及氨引起的星形胶质细胞水肿等细胞毒性效应的内容进行综述。

关键词: 肝性脑病, 氨中毒, 氧化应激, 能量代谢, 线粒体, 综述

Abstract: Ammonia toxicity has been generally accepted as one of the classic theories of the pathogenesis of hepatic encephalopathy (HE). Ammonia induces changes in neurological system energy metabolism, oxidative stress, mitochondrial permeability transition (MPT), GABA and Glutamatergic neurotransmission, intracellular signal transduction and Aquaporin 4 (AQP4) expression, astrocyte swelling is another important consequence of ammonia neurotoxicity. This article reviewed the role of these factors in the mechanism of HE and ammonia toxicity.

Key words: encephalopathy (HE), ammonia toxicity, oxidative stress, energy metabolism, mitochondrion, review