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作 者:廖月 何毅怀 罗亚文 LIAO Yue;HE Yihuai;LUO Yawen(Department of Infectious Diseases,Affiliated Hospital of Zunyi Medical University,Zunyi,Guizhou 563000,China)
机构地区:[1]遵义医科大学附属医院感染科,贵州遵义563000
出 处:《临床肝胆病杂志》2022年第10期2402-2407,共6页Journal of Clinical Hepatology
基 金:国家自然科学基金(82160370,81560110);贵州省科技计划项目(黔科合基础-ZK[2022]一般642)。
摘 要:急性肝损伤常由病毒感染、酒精、药物、毒物、代谢异常等原因引起。氧化应激是急性肝损伤及其他肝病发生发展的共同病理生理机制。急性肝损伤发生后,肝细胞功能受损,引起氧化应激;而持续或高强度的氧化应激将增加肝细胞死亡的风险,导致一系列肝脏疾病。氧化应激主要与Nrf2、NF-κB等信号通路相关。因此,了解氧化应激参与肝损伤的发生发展机制及相关通路至关重要。本文介绍了氧化系统及抗氧化系统、氧化应激与损伤因素、氧化应激与肝损伤相关通路,以期为急性肝损伤的治疗靶点选择及相关临床研究提供参考。Acute liver injury(ALI) is often caused by virus infection,alcohol,drugs,toxin,and metabolic disorder,and oxidative stress is a common pathophysiological mechanism in the development and progression of ALI and other liver diseases.Hepatocyte function is impaired after ALI,which further causes oxidative stress,and persistent or high-intensive oxidative stress may increase the risk of hepatocyte death and thus result in a series of liver diseases.Oxidative stress is mainly associated with the signaling pathways including nuclear factor erythroid 2-related factor 2 and nuclear factor-kappa B.Therefore,it is of great importance to understand the mechanism of oxidative stress in the development and progression of liver injury and related pathways.This article introduces oxidative system and antioxidative system,oxidative stress and damage factors,and oxidative stress and pathways associated with liver injury,so as to provide a reference for the selection of therapeutic targets for ALI and related clinical research.
关 键 词:急性肝损伤 氧化应激 NF-E2相关因子2 NF-ΚB
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