Mogroside V prevents ethanol-induced hangover and liver damage by reducing oxidative stress, steatosis and inflammation

Excessive alcohol consumption is a leading cause of alcohol-associated liver disease (ALD). Previous studies presented Mogroside V (MV) have protective effects on against nonalcoholic fatty liver disease. however, the effects of MV on ethanol-induced hangover and liver damage remains to be elucidated. Herein, we investigated the potential effects of MV in relieving hangover and mitigating liver injury induced by ethanol. MV significantly reduced blood ethanol, liver histological alterations and serum ALT, AST、TG levels in ethanol-treated mice. Moreover, MV accelerates alcohol metabolism by inhibiting the upregulation of CYP2E1 induced by ethanol, while enhancing the activity of ADH and ALDH, as well as upregulating the expression of ADH1 and ALDH2. MV mitigates oxidative stress by decreased hepatic malondialdehyde (MDA) levels, restored glutathione (GSH)、superoxide dismutase (SOD) and catalase (CAT) content in ethanol-induced mice. Mechanistically, MV activated the p-AMPK/SREBP-1/FASN pathway to decreased hepatic lipid accumulation and alleviated steatosis. Additionally, MV promoted nuclear translocation of Nrf-2 to attenuates oxidative stress and suppressed TLR4/MyD88/NF-κB signaling pathway to reduce Inflammatory responses triggered by ethanol in mice. In summary, this study highlights mogroside V's hangover relieving effect and its protective effects against ethanol-related liver damage through its lipid metabolism regulation, antioxidative action and anti-inflammatory properties. These results suggest that mogroside V could be developed as a potential therapeutic agent against ethanol-induced liver damage.