Cholesterol-lowering activity of 10-gingerol in HepG2 cells is associated with enhancing LDL cholesterol uptake, cholesterol efflux and bile acid excretion. (August 2022)

• Record Type: Journal Article
• Authors: Guo, Jingting; Li, Yawen; Yuan, Yangbing; Li, Xusheng; Li, Xiao; Jiang, Xinwei; Bai, Weibin; Jiao, Rui
• Is Part Of: Journal of functional foods. Volume 95(2022)
• Publication Date: 2022-08
• Subjects: Gingerol -- Cholesterol metabolism -- LDLR -- CYP7A1 -- Cholesterol efflux; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2022.105174
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: 10-GN showed the most effective cholesterol-lowering activity in HepG2 cells compared with 6-GN and 8-GN. 10-GN could enhance hepatic cholesterol uptake by up-regulating LDLR. 10-GN could promote cellular cholesterol efflux by increasing expressions of ABCG5/8 and ABCA1. 10-GN enhanced cellular bile acid excretion via up-regulating CYP7A1. Abstract: Gingerols including 6-gingerol, 8-gingerol and 10-gingerol are the pungent ingredients in ginger. Ginger extract and 6-gingerol have been reported to possess hypocholesterolemic activity. However, cholesterol-lowering activity of 8-gingerol and 10-gingerol has not been well investigated. The present study was to investigate effect of 8-gingerol and 10-gingerol on cholesterol level in HepG2 cells compared with 6-gingerol. HepG2 cells were incubated with 40 μM cholesterol and 4 μM 25-hydroxycholeterol with various concentrations of 6-gingerol, 8-gingerol or 10-gingerol, ranging from 0 to 100 μM for 24 h. It was found that 10-gingerol at 75 and 100 μM was more effective in decreasing cholesterol levels compared with 6-gingerol and 8-gingerol. Furthermore, 10-gingerol increased the expression of LDLR with a dose–response manner through up-regulating SREBP-2 and down-regulating PCSK9. 10-Gingerol also enhanced the expression of genes related to cholesterol efflux and bile acid expression including ABCG5/8 and ABCA1 through LXRα, PPARγ and CYP7A1 in HepG2 cells.