Nrf2在酒精性肝损伤模型中的研究进展  

Progress in research of Nrf2 in alcoholic liver injury models

作　　者：邢会杰[1,2] 宋琳亮[1] 方梅霞[1] 和君[1] 李守军[2] 傅江南[1] 

机构地区：[1]暨南大学实验动物管理中心,广州510632 [2]华南农业大学兽医学院,广州510642

出　　处：《中国比较医学杂志》2014年第4期74-77,共4页Chinese Journal of Comparative Medicine

基　　金：广东省科技基础条件建设项目(No.2011B060300015);国家自然基金(No.31101677)

摘　　要：氧化应激的产生与酒精性肝损伤的发生发展密切相关,目前被普遍认为是酒精性肝病的主要发病机制日益成为研究的热点。Nrf2是目前发现的抵御外源性刺激和毒物的抗氧化应答反应的核心途径之一,在许多药物或化学物质在体内的代谢解毒中具有重要作用,Nrf2的缺失或激活障碍,会加重氧化应激状态、破坏细胞内正常的氧化还原平衡稳态,导致细胞毒性、功能障碍、凋亡,甚至死亡。本文对Nrf2在酒精性肝损伤模型中的研究进行综述。The generation of oxidative stress is closely associated with the occurrence and development of liver injury induced by chronic alcohol consumption. It is widely considered that oxidative stress is the major mechanism of alcoholic liver disease has become a research hotspot. Nuclear factor erythroid 2-related factor 2 （Nrf2） is a key transcription factor that induces a battery of cytoprotective genes in response to oxidative/electrophilic insults. Nrf2 may play an important role in the metabolism and detoxification of a variety of drugs and chemical compounds. Deficiency of Nrf2 may aggravate the oxidative stress and damage homeostasis of redox system, resulting in cell toxicity, dysfunction, and even death. In this article we will review the research progress of Nrf2 in alcoholic liver injury models.

关 键 词：NRF2 酒精性肝损伤模型 氧化应激 

分 类 号：R33[医药卫生—人体生理学]