Background: Our previous study suggested that licorice has anti-inflammatory activity in lipopolysaccharide-stimulated microglial cells and anti-oxidative activity in tert-butyl hydroperoxide-induced oxidative liver damage. In this study, we evaluated the effect of licorice on chronic alcohol-induced fatty liver injury mediated by inflammation and oxidative stress. Methods: Raw licorice was extracted, and quantitative and qualitative analysis of its components was performed by using LC-MS/MS. Mice were fed a liquid alcohol diet with or without licorice for 4weeks. Results: We have standardized 70% fermented ethanol extracted licorice and confirmed by LC-MS/MS as glycyrrhizic acid (GA), 15.77±0.34μg/mg; liquiritin (LQ), 14.55±0.42μg/mg; and liquiritigenin (LG), 1.34±0.02μg/mg, respectively. Alcohol consumption increased serum alanine aminotransferase and aspartate aminotransferase activities and the levels of triglycerides and tumor necrosis factor (TNF)-aα. Lipid accumulation in the liver was also markedly induced, whereas the glutathione level was reduced. All these alcohol-induced changes were effectively inhibited by licorice treatment. In particular, the hepatic glutathione level was restored and alcohol-induced TNF-aα production was significantly inhibited by licorice. Conclusion: Taken together, our data suggests that protective effect of licorice against alcohol-induced liver injury may be attributed to its anti-inflammatory activity and enhancement of antioxidant defense.
- Alcohol-induced liver injury