谷胱甘肽在肝脏疾病相关信号通路中的作用及研究进展

发布时间：2018-05-28 13:23

本文选题：谷胱甘肽 + 肝脏疾病　；参考：《中国生物工程杂志》2015年10期

【摘要】：谷胱甘肽(GSH)是细胞内主要的抗氧剂和氧化还原、细胞信号调节器,它能还原过氧化氢、清除活性氧(ROS)和含氮自由基使细胞免受氧化应激损伤。不管细胞内是否存在ROS氧化细胞蛋白,谷胱甘肽均能诱导氧化还原反应发生转变,进一步使信号传导功能及转录因子分子功能发生改变。大量实验表明,ROS和GSH在多条细胞信号调节通路中发挥着重要作用。主要阐述了Fas、TNF-α和NF-κB信号通路及线粒体凋亡途径及GSH在这些通路中的作用。尤其是线粒体GSH耗竭能诱导线粒体内ROS显著增加,从而损害细胞生物能量和诱导线粒体通透性转换孔开启。根据线粒体损害程度,NF-κB信号通路可被抑制,肝细胞也可能经历不同的死亡模式(凋亡或坏死)并对刺激细胞死亡信号(如TNF-α)也更敏感。这些过程涉及许多肝脏疾病的发病机理。
[Abstract]:Glutathione (GSH) is the main antioxidant, redox, cell signal regulator, which can reduce hydrogen peroxide and scavenge reactive oxygen species (Ros) and nitrogen-containing free radicals to protect cells from oxidative stress. Glutathione can induce the redox reaction and change the signal transduction function and transcription factor molecular function, regardless of the existence of ROS oxidized cell protein or not. A large number of experiments show that Ros and GSH play an important role in many cell signaling pathways. The signaling pathway of Fas-TNF- 伪 and NF- 魏 B, mitochondrial apoptosis pathway and the role of GSH in these pathways were discussed. In particular, mitochondrial GSH depletion can induce a significant increase in ROS in mitochondria, which damages the biological energy of cells and induces the opening of mitochondrial permeability transition holes. According to the degree of mitochondrial damage, NF- 魏 B signaling pathway can be inhibited, and hepatocytes may undergo different death patterns (apoptosis or necrosis) and be more sensitive to stimulating cell death signals (such as TNF- 伪). These processes involve the pathogenesis of many liver diseases.
【作者单位】：江西中医药大学药学院;中国中医科学院中药研究所;
【基金】：国家“十二五”科技支撑计划课题资助项目(2011BAI04B01)
【分类号】：R575

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