Geniposide reduces cholesterol accumulation and increases its excretion by regulating the FXR-mediated liver-gut crosstalk of bile acids.

摘要: Abstract Hypercholesterolemia is the main risk factor to threaten human health and geniposide has been found have hypolipidemic functions. However, its underlying mechanism not clear. In this study, we firstly confirmed functions of in C57BL/6 ApoE−/− mice (i.p, 50 mg/kg/d). Then hepatic or arterial lipid accumulation was analyzed through histomorphology. Moreover, effects on bile acid metabolism were by RNA-seq biological molecular analysis. Mechanistically, GW4064, an FXR agonist, carried out verify mechanisms HepG2 Caco2 cells. As expected, decreased accumulations both plasma liver. Morever, atherosclerotic plaque shrank HCD-fed with treatment. The analysis revealed that accelerated synthesis acids inactivating negative feedback regulation mediated FXR, led enhancive reverse cholesterol transport catabolism. What’s more, reduced ileal FXR-mediated reabsorption acids, resulting increasing excretion acids. Our study pointed regulatory liver-gut crosstalk might be a novel strategy for maintaining homeostasis.