• GA mitigates alcohol-induced liver damage and oxidative stress in mice. • GA modulates gut microbiota composition and affects the liver via the gut-liver axis. • GA may ameliorate ALD by regulating the Metabolism of xenobiotics by cytochrome P450 and Glutathione metabolism pathways. • GA is a potential functional food ingredient for the treatment of alcoholic liver disease. The imbalance of gut microbiota ecology caused by alcohol consumption disrupts the gut-liver axis, leading to the occurrence and progression of alcoholic liver disease (ALD). This study investigates the effects of galangin (GA) on the gut-liver axis in an alcohol-induced mouse model of ALD, focusing on its potential to regulate gut microbiota composition, intestinal permeability, and hepatic inflammation. The results showed that GA intervention alleviated liver oxidative stress injury and inflammation, improved gut microbiota imbalance, regulated intestinal permeability by up-regulating the expression of tight junction proteins, and enhanced intestinal barrier function. GA treatment reduced liver oxidative stress and inflammation rectified, alcohol-induced dysbiosis, and bolstered the intestinal barrier by up-regulating tight junction proteins. Additionally, the improvement of ALD by GA is mainly related to the Metabolism of xenobiotics by cytochrome P450 and Glutathione metabolism pathways. These results suggest that GA may alleviate ALD by regulating abnormalities of the gut-liver axis.
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Duan et al. (2024) studied this question.
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