Affiliated Hospital of Taishan Medical University, Taian 271000, ChinaDepartment of Chemistry and Chemical Engineering, Weifang University, Weifang 261061, ChinaResearch Center on Life Sciences and Environmental Sciences, Harbin University of Commerce, Harbin 150076, ChinaSchool of Medicine and Pharmacy, Ocean University of China, Qingdao 266003, ChinaKey Laboratory of Atherosclerosis in Universities of Shandong Province, Institute of Atherosclerosis, Taishan Medical University, 2# Yingsheng East Road, Taian, Shandong Province 271000, China
Background: Quercetin, one of the most widely distributed flavonoids in plants, has been demonstrated to reduce hyperlipidaemia and atherosclerotic lesion formation. Reverse cholesterol transport 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 mic...更多
Background: Quercetin, one of the most widely distributed flavonoids in plants, has been demonstrated to reduce hyperlipidaemia and atherosclerotic lesion formation. Reverse cholesterol transport 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 , liver , and bile and finally to the feces 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 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 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.收起
