Antihypertensive effects of the flavonoid quercetin

Pérez‐Vizcaíno, Francisco; Ding, Juan; Jiménez, Rosario; Santos‐Buelga, Celestino; Osuna, Antonio

doi:10.1016/s1734-1140(09)70008-8

Cited by 273 publications

(196 citation statements)

References 43 publications

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“…The presence of high levels of biologically active polyphenolic compounds, such as the flavonoids, is a likely health-promoting factor. Flavonoids have repeatedly been shown to improve cardiovascular diseases including hypertension, ischemic heart disease, and stroke (Hertog et al, 1993;Keli et al, 1996;Perez-Vizcaino et al, 2009). It has been further shown that flavonoids protect and improve endothelial function (Engler et al, 2004;Vita, 2005;Hodgson, 2006;Grassi et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Luteolinidin Protects the Postischemic Heart through CD38 Inhibition with Preservation of NAD(P)(H)

Boslett

Hemann

Zhao

et al. 2017

J Pharmacol Exp Ther

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We recently showed that ischemia/reperfusion (I/R) of the heart causes CD38 activation with resultant depletion of the cardiac NADP(H) pool, which is most marked in the endothelium. This NADP(H) depletion was shown to limit the production of nitric oxide by endothelial nitric oxide synthase (eNOS), which requires NADPH for nitric oxide production, resulting in greatly altered endothelial function. Therefore, intervention with CD38 inhibitors could reverse postischemic eNOS-mediated endothelial dysfunction. Here, we evaluated the potency of the CD38 inhibitor luteolinidin, an anthocyanidin, at blocking CD38 activity and preserving endothelial and myocardial function in the postischemic heart. Initially, we characterized luteolinidin as a CD38 inhibitor in vitro to determine its potency and mechanism of inhibition. We then tested luteolinidin in the ex vivo isolated heart model, where we determined luteolinidin uptake with aqueous and liposomal delivery methods. Optimal delivery methods were then further tested to determine the effect of luteolinidin on postischemic NAD(P)(H) and tetrahydrobiopterin levels. Finally, through nitric oxide synthase-dependent coronary flow and left ventricular functional measurements, we evaluated the efficacy of luteolinidin to protect vascular and contractile function, respectively, after I/R. With enhanced postischemic preservation of NADPH and tetrahydrobiopterin, there was a dose-dependent effect of luteolinidin on increasing recovery of endothelium-dependent vasodilatory function, as well as enhancing the recovery of left ventricular contractile function with increased myocardial salvage. Thus, luteolinidin is a potent CD38 inhibitor that protects the heart against I/R injury with preservation of eNOS function and prevention of endothelial dysfunction.

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Section: Discussionmentioning

confidence: 99%

Luteolinidin Protects the Postischemic Heart through CD38 Inhibition with Preservation of NAD(P)(H)

Boslett

Hemann

Zhao

et al. 2017

J Pharmacol Exp Ther

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“…Epidemiological studies, together with data from animal models and some clinical trials, suggest a role of dietary flavonoids in the prevention of CVD and other age-related chronic diseases (108)(109)(110) . The flavonol quercetin exhibits a wide range of physiological effects such as inhibition of LDL-oxidation, lowering of arterial blood pressure and platelet aggregation, and improvement of endothelial function as shown in animal models and in human subjects (111)(112)(113)(114)(115)(116)(117) . Furthermore, cell culture and animal studies indicate a potent anti-inflammatory activity of quercetin (116,(118)(119)(120) .…”

Section: Flavonoidsmentioning

confidence: 99%

ApoE genotype: from geographic distribution to function and responsiveness to dietary factors

2012

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ApoE is a key protein in lipid metabolism with three major isoforms. ApoE allele frequencies show non-random global distribution especially in Europe with high apoE e3 frequency in the Mediterranean area, whereas the apoE e4 genotype is enriched in Northern Europe. The apoE e4 genotype is one of the most important genetic risk factors for age-dependent chronic diseases, including CVD and Alzheimer's disease (AD). The apoE polymorphism has been shown to impact on blood lipids, biomarkers of oxidative stress and chronic inflammation, which all may contribute to the isoform-dependent disease risk. Studies in mice and human subjects indicate that the apoE e3 but not the apoE e4 genotype may significantly benefit from dietary flavonoids (e.g. quercetin) and n-3 fatty acids. Metabolism of lipid soluble vitamins E and D is likewise differentially affected by the apoE genotype. Epidemiological and experimental evidence suggest a better vitamin D status in apoE e4 than e3 subjects indicating a certain advantage of e4 over e3. The present review aims at evaluation of current data available on interactions between apoE polymorphism and dietary responsiveness to flavonoids, fat soluble vitamins and n-3 fatty acids. Likewise, distinct geographic distribution and chronic disease risk of the different apoE isoforms are addressed.

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“…More recently, beneficial effects on blood pressure and heart disease have been described (Perez-Vizcaino et al 2009;Han et al 2009;Jung et al 2013). With regard to obesity, very little work has been carried out to date.…”

Section: Introductionmentioning

confidence: 99%

Quercetin can reduce insulin resistance without decreasing adipose tissue and skeletal muscle fat accumulation

et al. 2013

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Quercetin exhibits a wide range of biological functions. The first aim of the present work was to analyze the effects of quercetin on fat accumulation in adipose tissue and glycemic control in rats. Any potential involvement of muscle fatty acid oxidation in its effect on glycemic control was also assessed. Animals were fed a high-fat high-sucrose diet either supplemented with quercetin (30 mg/kg body weight/day), or not supplemented, for 6 weeks. One week before killing, a glucose tolerance test was carried out. Muscle triacylglycerol content, serum glucose, insulin, fructosamine and free fatty acids were measured, and homeostatic model assessment for insulin resistance (HOMA-IR) was calculated. The activities of lipogenic enzymes and lipoprotein lipase in adipose tissue, carnitine palmitoyl transferase-1b (CPT-1b) and citrate synthase in skeletal muscle, and the expression of several genes, ACO, CD36, CPT-1b, PPAR-a, PGC-1a, UCP 3 , TFAM and COX-2 in skeletal muscle were analyzed. Quercetin caused no significant reduction in body weight or adipose tissue sizes. However, fructosamine, basal glucose and insulin, and consequently HOMA-IR, were significantly reduced by quercetin. No changes were observed in the activity of lipogenic enzymes and lipoprotein lipase. Muscle triacylglycerol content was similar in both experimental groups. The expression of ACO, CD36, CPT-1b, PPAR-a, PGC-1a, UCP 3 , TFAM and COX-2 remained unchanged. It can be concluded that quercetin is more effective as an anti-diabetic than as an anti-obesity biomolecule. The improvement in insulin resistance induced by this flavonoid is not mediated by a delipidating effect in skeletal muscle.

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Antihypertensive effects of the flavonoid quercetin

Cited by 273 publications

References 43 publications

Luteolinidin Protects the Postischemic Heart through CD38 Inhibition with Preservation of NAD(P)(H)

Luteolinidin Protects the Postischemic Heart through CD38 Inhibition with Preservation of NAD(P)(H)

ApoE genotype: from geographic distribution to function and responsiveness to dietary factors

Quercetin can reduce insulin resistance without decreasing adipose tissue and skeletal muscle fat accumulation

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