| Summary: | In this work, we established a HepG2 cell model of hypercholesterolemia in order to investigate the cholesterol-lowering activity and underlying mechanism of sterols. The levels of total cholesterol (TC), triglycerides (TG) and cholesterol regulation-related proteins were measured in HepG2 cells treated with nothing, simvastatin as a positive control or sterols. The results showed that the four sterol compounds tested could reduce TC and TG levels and mitigate the increase of lipids levels and lipid metabolism disorder in hypercholesterolemic cells. Moreover, they reduced the biosynthesis and absorption of cholesterol, decreased cholesterol esterification and promoted cholesterol excretion to the intestine by down-regulating the expression of Niemann-Pick C1-like 1 (NPC1L1), acetyl-coenzyme A acetyltransferase 2 (ACAT2), 3-hydroxy-3-methylglutaryl-coenzyme A synthase (HMGCS1) and sterol-regulatory element-binding proteins (SREBP2), and up-regulating the expression of ATP-binding cassette transporter G5/8 (ABCG5/8). We concluded that sterols improve lipid levels in hypercholesterolemic cells by affecting the expression of proteins related to cholesterol absorption and metabolism.
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