Oxidative stress in alcoholic liver disease: Role of NADPH oxidase complex
Oxidative stress in alcoholic liver disease: Role of NADPH oxidase complex
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DOI：
10.1111/j.1440-1746.2007.05277.x
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发表时间：
2008-03-01
影响因子：
4.1
通讯作者：
Brenner, David A.
中科院分区：
文献类型：
--
作者：
De Minicis, Samele;Brenner, David A.
酒精是众所周知的肝损伤危险因素，也是全球肝病的主要原因之一。长期摄入酒精，超过一定限度，不可避免地导致肝脂肪变性。如果损伤持续，伴随肿瘤坏死因子-a和其他细胞因子的脂肪变性进展为脂肪性肝炎、纤维化和最终肝硬化。在参与酒精性肝损伤过程的多种因素中，氧化应激起着至关重要的作用。乙醇代谢过程中的几种机制导致活性氧（ROS）的产生。虽然酒精代谢的主要部位是肝细胞，但酒精诱导的肝损伤还涉及其他机制。具体而言，在ROS产生活性中，NADPH氧化酶复合物发挥重要作用。NADPH氧化酶在肝的肝细胞、肝星状细胞和枯否细胞中表达。研究NADPH氧化酶为酒精性肝损伤提供了新的见解，并为未来的治疗策略提供了新的方向。
Alcohol is a well-known risk factor for liver damage and is one of the major causes of liver disease worldwide. Chronic intake of alcohol, over a certain limit, inevitably leads to hepatic steatosis. If the injury persists, steatosis with concomitant tumor necrosis factor-a and other cytokines, progresses to steatohepatitis, fibrosis and finally cirrhosis. Among the multiple factors involved in the process of alcohol-induced liver injury, a crucial role is played by oxidative stress. Several mechanisms during ethanol metabolism result in reactive oxygen species (ROS) production. Although the main site of ethanol metabolism is hepatocytes, other mechanisms are involved in alcohol-induced liver injury. Specifically, in the ROS production activity, an important role is played by the NADPH oxidase complex. NADPH oxidase is expressed in hepatocytes, hepatic stellate cells and Kupffer cells in the liver. Studying NADPH oxidase gives new insights into alcohol-induced liver damage and provides new direction for future therapeutic strategies.