Pharmacological inhibition of NOX4 ameliorates alcohol-induced liver injury in mice through improving oxidative stress and mitochondrial function

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• 作者：Qian Sun^a ; ^b ; ¹ ; Wenliang Zhang^b ; ¹ ; Wei Zhong^b ; Xinguo Sun^b ; Zhanxiang Zhou^a ; ^b ; ^{z_zhou@uncg.edu}
• 关键词：Alcoholic liver disease ; Mitochondria ; NADPH oxidase ; NOX4 ; GKT137831 ; ROS
• 刊名：Biochimica et Biophysica Acta (BBA) - General Subjects
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：1861
• 期：1
• 页码：2912-2921
• 全文大小：2175 K
• 卷排序：1861

文摘

NOX4 predominantly localizes in the mitochondria in the liver of mice, and chronic alcohol exposure increases hepatic NOX4. Inhibition of NOX4 activity decreases alcohol-elevated serum hydrogen peroxide levels. Inhibition of NOX4 activity decreases alcohol-induced fat accumulation but increases HNF-4α and CPT-1 in the liver. Inhibition of NOX4 activity decreases alcohol-induced mitochondrial apoptotic cell death pathway. Knockdown of NOX4 protects against ethanol-induced loss of mitochondrial membrane potential and generation of ROS.