Monascus‐fermented red mold dioscorea protects mice against alcohol‐induced liver injury, whereas its metabolites ankaflavin and monascin regulate ethanol‐induced peroxisome proliferator‐activated receptor‐γ and sterol regulatory element‐binding transcription factor‐1 expression in HepG2 cells

BACKGROUND Alcoholic hepatitis is a necroinflammatory process that is associated with fibrosis and leads to cirrhosis in 40% of cases. The hepatoprotective effects of red mold dioscorea (RMD) from Monascus purpureus NTU 568 were evaluated in vivo using a mouse model of chronic alcohol‐induced liver disease (ALD). RESULTS ALD mice were orally administered vehicle (ALD group) or vehicle plus 307.5, 615.0 or 1537.5 mg kg–1 (1 ×, 2 × and 5 ×) RMD for 5 weeks. RMD lowered serum leptin, hepatic total cholesterol, free fatty acid and hepatic triglyceride levels and increased serum adiponectin, hepatic alcohol dehydrogenase and antioxidant enzyme levels. Furthermore, ankaflavin (AK) and monascin (MS), metabolites of RMD fermented with M. purpureus 568, induced peroxisome proliferator‐activated receptor‐γ expression and the concomitant suppression of ethanol‐induced elevation of sterol regulatory element‐binding transcription factor‐1 and TG in HepG2 cells. CONCLUSION These results indicate the hepatoprotective effect of Monascus‐fermented RMD. Moreover, AK and MS were identified as the active constituents of RMD for the first time and were shown to protect against ethanol‐induced liver damage. © 2017 Society of Chemical Industry