%A XUE Zhan-xia, PENG Liang
%T Research Progress on Hyperammonia-induced Hepatic Encepha-lopathy
%0 Journal Article
%D 2011
%J ACTA NEUROPHARMACOLOGICA
%R 
%P 33-41
%V 1
%N 4
%U {http://actanp.hebeinu.edu.cn/CN/abstract/article_40.shtml}
%8 2011-08-26
%X Hepatic encephalopathy （HE） is a serious complication of acute or chronic liver failure，caused by many reasons （i.e. ammonia，multiple neurotoxins，false neurotransmitters and benzodiazepine-like compounds）. Evidences suggest that ammonia plays a major role in pathogenesis of HE. Hyperammonia up-regulates gene expression of peripheral-type benzodiazepine receptor （PTBR），glucose tranporter-1 （GLUT-1），aquaporin-4 （AQP4），and Na<sup>+</sup>/K<sup>+</sup>-ATPase in astrocytes；alters the phosphorylation state of the microtubule-associated protein-2 （MAP-2） and the expression of N-methyl-D-aspartate （NMDA） receptor；induces increase of NO，therefore astrocytic disfunction. It was reported previously that ammonia increased production of ouabain-like compounds and Na<sup>+</sup>/K<sup>+</sup>-ATPase activity in astrocytes. Research to the relationship of these factors will help us to understand the underlying mechanisms of ammonia-induced astrocytic disfunction and eventually contribute to the new strategies of prevention and therapy of HE.