期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 65, 期 -, 页码 908-915出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2013.08.185
关键词
Polyphenol; Flavonoid; Quercetin; Endothelial function; Atherosclerosis; HO-1; NO; Oxidative stress
资金
- National Health & Medical Research Council (NHMRC) Project Grant [634387]
- Raine Medical Research Foundation Priming Grant
- China Scholarship Council
- University of Western Australia Scholarship
- National Heart Foundation of Australia Postdoctoral Fellowship
- Medical Research Foundation at Royal Perth Hospital
- NHMRC Senior Research Fellowship
- NHMRC Senior Principal Research Fellowship
Several lines of evidence indicate that quercetin, a polyphenol derived in the diet from fruit and vegetables, contributes to cardiovascular health. We aimed to investigate the effects of dietary quercetin on endothelial function and atherosclerosis in mice fed a high-fat diet. Wild-type C57BL/6 (WT) and apolipoprotein E gene knockout (ApoE(-/-)) mice were fed: (i) a high-fat diet (HFD) or (ii) a HFD supplemented with 0.05% w/w quercetin (HFD + Q), for 14 weeks. Compared with animals fed HFD, HFD+Q attenuated atherosclerosis in ApoE-/- mice. Treatment with the HFD+Q significantly improved endothelium-dependent relaxation of aortic rings isolated from WT but not ApoE-/- mice and attenuated hypochlorous acid-induced endothelial dysfunction in aortic rings of both WT and ApoE(-/-) mice. Mechanistic studies revealed that HFD + Q significantly improved plasma F-2-isoprostanes, 24 h urinary nitrite, and endothelial nitric oxide synthase activity, and increased heme oxygenase-1 (HO-1) protein expression in the aortas of both WT and ApoE-/- mice (P<0.05). HFD+Q also resulted in small changes in plasma cholesterol (P<0.05 in WT) and plasma triacylglycerols (P<0.05 in ApoE(-/-) mice). In a separate experiment, quercetin did not protect against hypochlorite-induced endothelial dysfunction in arteries obtained from heterozygous HO-1 gene knockout mice with low expression of HO-1 protein. Quercetin protects mice fed a HFD against oxidant-induced endothelial dysfunction and ApoE-/- mice against atherosclerosis. These effects are associated with improvements in nitric oxide bioavailability and are critically related to arterial induction of HO-1. (C) 2013 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据