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dc.contributor.authorJones, Huw S.
dc.contributor.authorGordon, A.
dc.contributor.authorMagwensi, S.G.
dc.contributor.authorNaseem, K.
dc.contributor.authorAtkin, S.L.
dc.contributor.authorCourts, F.L.
dc.date.accessioned2020-04-29T11:19:30Z
dc.date.accessioned2020-05-11T10:55:12Z
dc.date.available2020-04-29T11:19:30Z
dc.date.available2020-05-11T10:55:12Z
dc.date.issued2016-04
dc.identifier.citationJones HS, Gordon A, Magwenzi SG et al (2016) The dietary flavonol quercetin ameliorates angiotensin II-induced redox signaling imbalance in a human unbilical vein endothelial cell model of endothelial dysfunction via ablation of p47phox expression. Molecular Nutrition and Food Research. 60(4): 787-797.en_US
dc.identifier.urihttp://hdl.handle.net/10454/17790
dc.descriptionYesen_US
dc.description.abstractQuercetin is reported to reduce blood pressure in hypertensive but not normotensive humans, but the role of endothelial redox signaling in this phenomenon has not been assessed. This study investigated the effects of physiologically obtainable quercetin concentrations in a human primary cell model of endothelial dysfunction in order to elucidate the mechanism of action of its antihypertensive effects. Angiotensin II (100 nM, 8 h) induced dysfunction, characterized by suppressed nitric oxide availability (85 ± 4% p<0.05) and increased superoxide production (136 ± 5 %, p<0.001). These effects were ablated by an NADPH oxidase inhibitor. Quercetin (3 μM, 8 h) prevented angiotensin II induced changes in nitric oxide and superoxide levels, but no effect upon nitric oxide or superoxide in control cells. The NADPH oxidase subunit p47(phox) was increased at the mRNA and protein levels in angiotensin II-treated cells (130 ± 14% of control, p<0.05), which was ablated by quercetin co-treatment. Protein kinase C activity was increased after angiotensin II treatment (136 ± 51%), however this was unaffected by quercetin co-treatment. Physiologically obtainable quercetin concentrations are capable of ameliorating angiotensin II-induced endothelial nitric oxide and superoxide imbalance via protein kinase C-independent restoration of p47(phox) gene and protein expression.en_US
dc.description.sponsorshipInnovate UK and Boots Pharmaceuticalsen_US
dc.language.isoenen_US
dc.publisherWiley
dc.relation.isreferencedbyhttps://doi.org/10.1002/mnfr.201500751en_US
dc.rights© 2016 Wiley. This is the peer-reviewed version of the following article: Jones HS, Gordon A, Magwenzi SG et al (2016) The dietary flavonol quercetin ameliorates angiotensin II-induced redox signaling imbalance in a human unbilical vein endothelial cell model of endothelial dysfunction via ablation of p47phox expression. Molecular Nutrition and Food Research. 60(4): 787-797, which has been published in final form at https://doi.org/10.1002/mnfr.201500751. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.
dc.subjectEndothelial cellsen_US
dc.subjectNADPH oxidaseen_US
dc.subjectNitric oxideen_US
dc.subjectQuercetinen_US
dc.subjectSuperoxideen_US
dc.titleThe dietary flavonol quercetin ameliorates angiotensin II-induced redox signaling imbalance in a human unbilical vein endothelial cell model of endothelial dysfunction via ablation of p47phox expressionen_US
dc.status.refereedYesen_US
dc.date.Accepted2016-01-05
dc.date.application2016-01-17
dc.typeArticleen_US
dc.type.versionAccepted manuscripten_US
dc.date.updated2020-04-29T10:19:32Z
refterms.dateFOA2020-05-12T12:56:03Z


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