Abstract
Acetaldehyde is the major toxic metabolite of alcohol (ethanol) and enhances fibrosis of the liver through hepatic stellate cells. Additionally, alcohol administration causes the accumulation of reactive oxygen species (ROS), which induce hepatocyte injury-mediated lipid peroxidation. Iso-α-acids, called isohumulones, are bitter acids in beer. The purpose of this study was to investigate the protective effects of iso-α-acids against alcoholic liver injury in hepatocytes in mice. C57BL/6N mice were fed diets containing isomerized hop extract, which mainly consists of iso-α-acids. After 7 days of feeding, acetaldehyde was administered by a single intraperitoneal injection. The acetaldehyde-induced increases in serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were suppressed by iso-α-acids intake. Hepatic gene expression analyses showed the upregulation of detoxifying enzyme genes, glutathione-S-transferase (GST) and aldehyde dehydrogenase (ALDH). In vitro, iso-α-acids upregulated the enzymatic activities of GST and ALDH and induced the nuclear translocation of nuclear factor-erythroid-2-related factor 2 (Nfe2l2; Nrf2), a master regulator of antioxidant and detoxifying systems. These results suggest that iso-α-acid intake prevents acetaldehyde-induced liver injury by reducing oxidative stress via Nrf2-mediated gene expression.
Highlights
Excessive consumption of alcoholic beverages is a leading cause of liver disease, including cirrhosis, liver cancer, and acute and chronic liver failure, worldwide [1]
This result suggested that the intake of iso-α-acids provided preventive effects in mouse liver against acetaldehyde-induced injury
To select differentially expressed genes (DEGs) related to liver injury, we focused on the upregulated genes including Gene Ontology (GO) terms related to “glutathione metabolic process (GO:0006749)” (Table 1)
Summary
Excessive consumption of alcoholic beverages is a leading cause of liver disease, including cirrhosis, liver cancer, and acute and chronic liver failure, worldwide [1]. The metabolism of ethanol generates reactive oxygen species (ROS), which play a role in the deterioration of alcoholic liver disease (ALD) [2]. There was a positive correlation between individual alcohol consumption and the ratio of ALD patients to all liver disease patients, and both are increasing in Asia [3]. In 2010, alcohol-attributable liver cirrhosis was responsible for 493,300 deaths. Alcohol-attributable liver cirrhosis was responsible for 225,900 deaths in Asia [3].
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