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Monascus-fermented red mold dioscorea protects mice against alcohol-induced liver injury, while its metabolites ankaflavin and monascin regulates ethanol induced PPAR-γ and SREBP-1 expression in HepG2 cells.

Monascus-fermented red mold dioscorea protects mice against alcohol-induced liver injury, while its metabolites ankaflavin and monascin regulates ethanol induced PPAR-γ and SREBP-1 expression in HepG2 cells.
Author Information (click to view)

Cheng CF, Pan TM,


Cheng CF, Pan TM, (click to view)

Cheng CF, Pan TM,

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Journal of the science of food and agriculture 2017 09 13() doi 10.1002/jsfa.8670
Abstract
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 (TG) 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 (PPAR)-γ expression and the concomitant suppression of ethanol-induced elevation of sterol regulatory element-binding transcription factor (SREBP)-1 and TG in HepG2 cells.

CONCLUSION
These results indicated 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.

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