ACTA NEUROPHARMACOLOGICA ›› 2011, Vol. 1 ›› Issue (4): 33-41.

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Research Progress on Hyperammonia-induced Hepatic Encepha-lopathy

XUE Zhan-xia1,PENG Liang2   

  1. 1. Department of Pharmacology,Hebei North University,Zhangjiakou,075000,China
    2. Department of Clinical Pharmacology,China Medical University,Shenyang,110001,China
  • Online:2011-08-26 Published:2012-11-24

Abstract: 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+/K+-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+/K+-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.

Key words: hepatic encephalopathy (HE), peripheral-type benzodiazepine receptor(PTBR), glucose tranporter-1(GLUT-1), aquaporin-4(AQP4), Na+/K+-ATPase, microtubule-associated protein(MAP-2), N-methyl-D-aspartate (NMDA) receptor, nitric oxide (NO)

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