Our results indicate that the hypocholesterolemic activity of cyanidin-3-O-β-glucoside was, at least in part, mediated by activating the potential LXRα-CYP7A1-bile acid excretion pathway, thus contributing to the antiatherogenic effect of cyanidin-3-O-β-glucoside. Importantly, cyanidin-3-O-β-glucoside could activate LXRα in an agonist-dependent manner.

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Lecithin cholesterol acyltransferase (LCAT) is a key enzyme in the metabolism of high density lipoprotein (HDL), which has been found inversely correlated with atherosclerosis. Adenovirus mediated overexpression of human LCAT (hLCAT) in hamsters resulted in increased levels of plasma total cholesterol, HDL cholesterol, phospholipids and enlarged particle size of HDL. It also increased cholesterol and total bile acid concentrations in bile. Hepatic mRNA level of cholesterol 7a-hydroxylase increased 2.7-fold in hamsters. However, such effects were not observed in mice in a parallel experiment. This study suggests that overexpression of hLCAT in hamsters facilitated reverse cholesterol transport. Similar metabolic changes in humans might modify atherogenic risk.

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