Abstract
Ankaflavin (AK) is a yellow pigment isolated from Monascus-fermented product. The potential mechanism of AK-regulated dyslipidemia in high-fat diet hamsters was investigated. The results showed that AK treatment reduced plasma total cholesterol (TC) level in hamsters, elevated faecal TC and bile acid concentration, and protected high density apolipoprotein-cholesterol (HDL-C) from diminishing. We further used hepatocytes to demonstrate that AK stabilized HDL levels via nuclear factor-erythroid 2 related factor 2 (Nrf2) activation and downstream molecule haem oxygenase-1 (HO-1) expression, as well as increasing liver x receptor-α (LXRα) mRNA level to promote ATP-binding cassette transporter (ABCA1) and apolipoprotein-A1 (apo-A1) expression. AK increased low density apolipoprotein-cholesterol (LDL-C) expression to promote cholesterol absorption in hepatocytes, and resulted in cholesterol metabolism by cytochrome P450 7A1 (CYP7A1), leading to the conversion of cholesterol into bile acid. Taken together, AK may serve as a cholesterol lowering agent to improve dyslipidemia.
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