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    Dietary quercetin attenuates oxidant-induced endothelial dysfunction and atherosclerosis in apolipoprotein e knockout mice fed a high-fat diet: A critical role for heme oxygenase-1

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    Fulltext not available
    Authors
    Shen, Y.
    Ward, Natalie
    Hodgson, J.
    Puddey, I.
    Wang, Y.
    Zhang, D.
    Maghzal, G.
    Stocker, R.
    Croft, K.
    Date
    2013
    Type
    Journal Article
    
    Metadata
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    Citation
    Shen, Y. and Ward, N. and Hodgson, J. and Puddey, I. and Wang, Y. and Zhang, D. and Maghzal, G. et al. 2013. Dietary quercetin attenuates oxidant-induced endothelial dysfunction and atherosclerosis in apolipoprotein e knockout mice fed a high-fat diet: A critical role for heme oxygenase-1. Free Radical Biology and Medicine. 65: pp. 908-915.
    Source Title
    Free Radical Biology and Medicine
    DOI
    10.1016/j.freeradbiomed.2013.08.185
    ISSN
    0891-5849
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/10995
    Collection
    • Curtin Research Publications
    Abstract

    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 F2-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.

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