Although emerging evidence demonstrated that quercetin could be explored as a potential candidate for the early intervention of alcoholic liver disease (ALD), the exact mechanisms against ethanol-induced hepatic steatosis haven't been fully elucidated. Herein, we investigated the effect of quercetin on liver steatosis caused by chronic-plus-single-binge ethanol feeding, focusing on lipophagy. Adult male mice were pair-fed with liquid diets containing ethanol (28% of total calories) and treated with quercetin for 12 weeks. Chronic-plus-binge ethanol consumption led to lipid droplets accumulation and liver damage as evidenced by histopathological changes, the increased content of triglyceride in serum and liver, and the elevated of serum ALT and AST level, which were greatly attenuated by quercetin. Moreover, quercetin blocked autophagy suppression by chronic-binge ethanol intake as manifested by the morphological improvement of mitochondrial characteristics, the increased number of autolysosome and restoration of autophagy-related protein expression. Furthermore, quercetin promoted lipophagy confirmed by the decreased perilipin 2 (PLIN2) level, activated AMPK activity and increased co-localization of liver LC3II and PLIN2 proteins. Collectively, these findings suggest that regular consumption of dietary quercetin has a role in preventing hepatic steatosis induced by chronic-plus-binge ethanol feeding, which mechanism may associate with the evident regulatory effect of quercetin on lipophagy.
Keywords: Alcoholic liver disease (ALD); Lipophagy; Perilipin 2 (PLIN2); Quercetin.
Copyright © 2018. Published by Elsevier Ltd.