Quercetin and its metabolites improve vessel function by inducing eNOS activity via phosphorylation of AMPK

Y. Shen, Kevin Croft, Jonathan Hodgson, Reece Kyle, I.-L.E. Lee, Y. Wang, R. Stocker, Natalie Ward

Research output: Contribution to journalArticlepeer-review

90 Citations (Scopus)

Abstract

[Truncated abstract] Quercetin is a major flavonoid in a wide range of fruits and vegetables. Consumption of quercetin may contribute to a reduction in risk of cardiovascular disease (CVD). Following ingestion, flavonoids are metabolized rapidly by methylation or glucuronidation, which can alter their biological activity. Certain dietary flavonoids have been shown to upregulate the expression of adenosine monophosphate-activated protein kinase (AMPK). AMPK is a conserved key enzyme in cellular energy homeostasis that affects fatty acid oxidation. The aim of the present study was to investigate the effects of supraphysiological concentrations of quercetin and its methyl and glucuronide metabolites (3′-O-methyl-quercetin and quercetin-3-O-glucuronide) on activation of AMPK and eNOS in human aortic endothelial cells (HAECs) and endothelial function in isolated aortic rings from C57BL mice. We found that 5 and 10 μM quercetin and its metabolites, and pretreatment of arteries with quercetin and its metabolites can protect vessels against hypochlorous acid-induced endothelial dysfunction in isolated arteries (P <0.05). Inhibition of AMPK blocked these protective effects....
Original languageEnglish
Pages (from-to)1036-1044
JournalBiochemical Pharmacology
Volume84
Issue number8
Early online date28 Jul 2012
DOIs
Publication statusPublished - Oct 2012

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