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. 2017 Jan 14;16(1):9.
doi: 10.1186/s12944-016-0393-2.

Quercetin improves macrophage reverse cholesterol transport in apolipoprotein E-deficient mice fed a high-fat diet

Yingjie Cui  1 , Pengbo Hou  1   2 , Fahui Li  3 , Qinghua Liu  4 , Shucun Qin  5 , Guanghai Zhou  1 , Xuelian Xu  6 , Yanhong Si  1 , Shoudong Guo  7
Affiliations

Quercetin improves macrophage reverse cholesterol transport in apolipoprotein E-deficient mice fed a high-fat diet

Yingjie Cui et al. Lipids Health Dis. .

Abstract

Background: Quercetin, one of the most widely distributed flavonoids in plants, has been demonstrated to reduce hyperlipidaemia and atherosclerotic lesion formation. Reverse cholesterol transport (RCT) plays a crucial role in exporting cholesterol from peripheral cells, which is one mechanism utilized in the prevention and treatment of atherosclerosis. The aim of this study is to investigate whether quercetin reduces lipid accumulation by improving RCT in vivo.

Methods: Apolipoprotein E-deficient mice fed a high-fat diet were used to investigate the effect of quercetin on RCT by an isotope tracing method, and the underlying mechanisms were clarified by molecular techniques.

Results: These novel results demonstrated that quercetin significantly improved [3H]-cholesterol transfer from [3H]-cholesterol-loaded macrophages to the plasma (approximately 34% increase), liver (30% increase), and bile (50% increase) and finally to the feces (approximately 40% increase) for excretion in apolipoprotein E-deficient mice fed a high-fat diet. Furthermore, quercetin markedly increased the cholesterol accepting ability of plasma and high-density lipoprotein (HDL) and dramatically decreased the content of malondialdehyde in plasma and oxidized phosphocholine carried by HDL. Therefore, the underlying mechanisms of quercetin in improving RCT may be partially due to the elevated cholesterol accepting ability of HDL, the increased expression levels of proteins related to RCT, such as ATP-binding cassettes (ABC) A1 and G1, and the improved antioxidant activity of HDL.

Conclusion: Quercetin accelerates RCT in an atherosclerosis model, which is helpful in clarifying the lipid-lowering effect of quercetin.

Keywords: Animal; Atherosclerosis; Cholesterol; Diet; LC-MS/MS; Medicine.

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Figures

Fig. 1
Fig. 1
Quercetin improves reverse cholesterol transport in apoE −/− mice (n = 6). a Quercetin increases the transfer rate of [3H]-cholesterol from injected foam macrophages to the plasma of apoE −/− mice; (b) [3H]-cholesterol in the liver of the apoE −/− mice after 48 h injection; (c) [3H]-cholesterol in the bile of the apoE −/− mice after 48 h injection; (d) [3H]-cholesterol in the faeces of the apoE −/− mice; (e) in vitro [3H]-cholesterol efflux assay using plasma as acceptor; (f) in vitro [3H]-cholesterol efflux assay using HDL particles as acceptor; (g) levels of plasma MDA as measured by assay kit; (h) levels of oxidized phosphocholines as measured by LC-MS/MS. CMCNa: carboxymethyl cellulose sodium. Data are expressed as the mean ± SD. & p < 0.05 vs CMCNa group; && p < 0.01 vs CMCNa group
Fig. 2
Fig. 2
Quercetin improves cholesterol efflux and the protein expression of ABCA1 and ABCG1 in Raw264.7 macrophages (n = 3). a Quercetin improves [3H]-cholesterol efflux in a concentration-dependent manner; (b) protein expression of SR-B1 and densitometric quantification; (c) protein expression of ABCA1 and densitometric quantification; (d) protein expression of ABCG1 and densitometric quantification; (e) quercetin improves the protein expression of ABCG1 in a concentration-dependent manner. Data are expressed as the mean ± SD. & p < 0.05 vs blank group; && p < 0.01 vs blank group
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