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肝脏疾病潜在的氧化应激信号传导及肝脏保护机制。

Oxidative stress signaling underlying liver disease and hepatoprotective mechanisms.

作者信息

Videla Luis A

机构信息

Luis A Videla, Molecular and Clinical Pharmacology Program, Institute of Biomedical Sciences, Faculty of Medicine, University of Chile, Santiago-7, Chile.

出版信息

World J Hepatol. 2009 Oct 31;1(1):72-8. doi: 10.4254/wjh.v1.i1.72.

Abstract

Oxidative stress is a redox imbalance between pro-oxidants and antioxidants in favour of the former ones, leading to different responses depending on the level of pro-oxidants and the duration of the exposure. In this article, we discuss the damaging or cytoprotective signaling mechanisms associated with oxidative stress by addressing (1) the role of prolonged and severe oxidative stress and insulin resistance as determinant factors in the pathogenesis of non-alcoholic fatty liver disease associated with obesity, which, with the concurrence of nutritional factors, may determine the onset of fatty liver and its progression to steatohepatitis; and (2) the development of an acute and mild pro-oxidant state by thyroid hormone administration, which elicits the redox up-regulation of the expression of proteins affording cell protection, as a preconditioning strategy against ischemia-reperfusion liver injury.

摘要

氧化应激是促氧化剂和抗氧化剂之间的氧化还原失衡,且这种失衡有利于前者,这会导致根据促氧化剂水平和暴露持续时间产生不同的反应。在本文中,我们通过探讨以下内容来讨论与氧化应激相关的损伤或细胞保护信号机制:(1)长期和严重氧化应激及胰岛素抵抗作为肥胖相关非酒精性脂肪性肝病发病机制中的决定因素所起的作用,在营养因素的共同作用下,这些因素可能决定脂肪肝的发生及其向脂肪性肝炎的进展;(2)通过给予甲状腺激素产生急性和轻度促氧化剂状态,这会引发具有细胞保护作用的蛋白质表达的氧化还原上调,作为针对缺血再灌注肝损伤的预处理策略。

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