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肝性脑病的变化面貌:炎症和氧化应激的作用。

Changing face of hepatic encephalopathy: role of inflammation and oxidative stress.

出版信息

World J Gastroenterol. 2010 Jul 21;16(27):3347-57. doi: 10.3748/wjg.v16.i27.3347.

Abstract

The face of hepatic encephalopathy (HE) is changing. This review explores how this neurocognitive disorder, which is associated with both acute and chronic liver injury, has grown to become a dynamic syndrome that spans a spectrum of neuropsychological impairment, from normal performance to coma. The central role of ammonia in the pathogenesis of HE remains incontrovertible. However, over the past 10 years, the HE community has begun to characterise the key roles of inflammation, infection, and oxidative/nitrosative stress in modulating the pathophysiological effects of ammonia on the astrocyte. This review explores the current thoughts and evidence base in this area and discusses the potential role of existing and novel therapies that might abrogate the oxidative and nitrosative stresses inflicted on the brain in patients with, or at risk of developing, HE.

摘要

肝性脑病(HE)的表现正在发生变化。本综述探讨了这种与急性和慢性肝损伤都有关的神经认知障碍如何发展成为一种动态综合征,涵盖了从正常表现到昏迷的一系列神经心理损伤。氨在 HE 发病机制中的核心作用仍然不可动摇。然而,在过去的 10 年中,HE 领域的研究人员已经开始描述炎症、感染和氧化/硝化应激在调节氨对星形胶质细胞的病理生理影响方面的关键作用。本综述探讨了该领域目前的思路和证据基础,并讨论了现有和新型疗法在减轻处于或有发生 HE 风险的患者大脑所遭受的氧化和硝化应激方面的潜在作用。

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