Genistein Protects against Acetaldehyde-Induced Oxidative Stress and Hepatocyte Injury in Chronic Alcohol-Fed Mice

染料木素 乙醛 氧化应激 酒精性肝病 肝损伤 乙醇代谢 化学 肝细胞 内分泌学 血红素加氧酶 醇脱氢酶 内科学 CYP2E1 药理学 血红素 生物化学 医学 乙醇 细胞色素P450 新陈代谢 肝硬化 体外
作者
Qinchao Ding,Aiwen Pi,Liuyi Hao,Tiantian Xu,Qin Zhu,Long Shu,Xiao-Long Yu,Wei-Guang Wang,Caijuan Si,Songtao Li
出处
期刊:Journal of Agricultural and Food Chemistry [American Chemical Society]
卷期号:71 (4): 1930-1943 被引量:8
标识
DOI:10.1021/acs.jafc.2c05747
摘要

Alcohol-related liver disease (ALD) is one of the most prevalent forms of liver disease in the world. Acetaldehyde, an intermediate product of alcohol catabolism, is a cause of liver injury caused by alcohol. This study was designed to evaluate the protective role and mechanism(s) of genistein against acetaldehyde-induced liver injury in the pathological process of ALD. We found that genistein administration significantly ameliorated alcohol-induced hepatic steatosis, injury, and inflammation in mice. Genistein supplementation markedly reversed hepatic oxidative stress, endoplasmic reticulum stress, mitochondrial dysfunction, and hepatocellular apoptosis in both alcohol-fed mice liver and acetaldehyde-treated hepatocytes. The mechanistic experiments revealed that the restoration of genistein administration rescued heme oxygenase-1 (HO-1) reduction at both transcriptional and protein levels in either alcohol-fed mice liver or acetaldehyde-treated hepatocytes, and the beneficial aspects derived from genistein were abolished in antioxidase heme oxygenase-1 (HO-1)-deficient hepatocytes. Moreover, we confirmed that genistein administration-restored hepatic nuclear factor erythroid 2-related factor 2 (NRF2), a key transcriptional regulator of HO-1, was involved in the protective role of genistein in ALD. This study demonstrated that genistein ameliorated acetaldehyde-induced oxidative stress and liver injury by restoring the hepatic NRF2-HO-1 signaling pathway in response to chronic alcohol consumption. Therefore, genistein may serve as a potential therapeutic choice for the treatment of ALD.
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