Alcohol metabolism causes an excessive accumulation of liver
lipids and
inflammation, resulting in liver damage. The yellow pigments
monascin (MS) and
ankaflavin (AK) of Monascus purpureus-fermented rice were proven to regulate
ethanol-induced damage in HepG2 cells, but the complete anti-inflammatory and anti-
fatty liver mechanisms in the animal model are still unclear. This study explored the roles of MS and AK in improving alcoholic liver injury. MS and AK were simultaneously fed to evaluate their effects and mechanisms in C57BL/6J mice fed the Lieber-DeCarli liquid alcohol diet for 6 weeks. The results indicated that MS and AK significantly reduced the serum
aspartate aminotransferase and
alanine aminotransferase activity, as well as the total liver
cholesterol and
triglyceride levels. The histopathological results indicated that MS and AK prevented
lipid accumulation in the liver. MS and AK effectively enhanced the activity of
antioxidant enzymes and reduced the degree of lipid peroxidation; AK was particularly effective and exhibited a superior preventive effect against alcoholic liver injury and
fatty liver. In addition to inhibiting the phosphorylation of the MAPK family, MS and AK directly reduced TNF-α,
IL-6, and IL-1β levels, thereby reducing NF-κB and its downstream iNOS and COX-2 expressions, as well as increasing
PPAR-γ, Nrf-2, and HO-1 expressions to prevent liver damage. MS and AK also directly reduced TNF-α,
IL-6, and IL-1β expression, thereby reducing the production of NF-κB and its downstream iNOS and COX-2, and increasing
PPAR-γ, Nrf-2, and HO-1 expressions, preventing alcohol damage to the liver.