Dietary quercetin attenuates oxidant-induced endothelial dysfunction and atherosclerosis in apolipop

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Background Atherosclerosis is the major contributor to cardiovascular disease, the leading cause of morbidity and mortality in developed countries.Chronic endothelial dysfunction is an early and independent predictor of cardiovascular disease.Given its pivotal role in the atherogenic process, endothelial dysfunction may be regarded as a critical risk factor indicating the existence of a specific atherogenic vascular milieu.Long and short-term intervention studies using polyphenol-rich foods including fruit, cocoa, tea and red wine have shown cardiovascular protective effects.Quercetin is one of the most important polyphenols existing ubiquitously in fruit and vegetables.Recently, we have demonstrated that intake of specific flavonoids such as quercetin and epicatechin can increase nitric oxide (NO) production and improve endothelial function in healthy subjects.Heme oxygenase-1 (HO-1) is the inducible form of heme oxygenases.It exerts anti-inflammatory and antioxidant activity within the vasculature, and its induction can protect against reactive oxygen species (ROS)-induced oxidative damage.We hypothesized that chronic consumption of quercetin can improve endothelial function and attenuate atherosclerosis by up-regulating eNOS activity and increasing subsequent NO production, and inducing HO-1.Here we assess the effect of chronic quercetin consumption on HOCl-induced vascular dysfunction and atherosclerosis development in ApoE-/-and wild-type C57B1 (WT) mice fed a high fat diet.
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