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dc.contributor.authorMorales-Cano, Daniel
dc.contributor.authorMenéndez, Carmen
dc.contributor.authorMoreno, Enrique
dc.contributor.authorMoral-Sanz, Javier
dc.contributor.authorBarreira, Bianca
dc.contributor.authorGalindo Gallardo, Pilar
dc.contributor.authorPandolfi, Rachele
dc.contributor.authorJiménez, Rosario
dc.contributor.authorMoreno, Laura
dc.contributor.authorCogolludo, Ángel
dc.contributor.authorDuarte Pérez, Juan Manuel 
dc.contributor.authorPérez-Vizcaíno, Francisco
dc.date.accessioned2015-02-19T14:02:00Z
dc.date.available2015-02-19T14:02:00Z
dc.date.issued2014
dc.identifier.citationMorales-Cano, D.; et al. The Flavonoid Quercetin Reverses Pulmonary Hypertension in Rats. Plos One, 9(12): e114492 (2014). [http://hdl.handle.net/10481/34881]es_ES
dc.identifier.issn1932-6203es_ES
dc.identifier.urihttp://hdl.handle.net/10481/34881
dc.description.abstractQuercetin is a dietary flavonoid which exerts vasodilator, antiplatelet and antiproliferative effects and reduces blood pressure, oxidative status and end-organ damage in humans and animal models of systemic hypertension. We hypothesized that oral quercetin treatment might be protective in a rat model of pulmonary arterial hypertension. Three weeks after injection of monocrotaline, quercetin (10 mg/kg/d per os) or vehicle was administered for 10 days to adult Wistar rats. Quercetin significantly reduced mortality. In surviving animals, quercetin decreased pulmonary arterial pressure, right ventricular hypertrophy and muscularization of small pulmonary arteries. Classic biomarkers of pulmonary arterial hypertension such as the downregulated expression of lung BMPR2, Kv1.5, Kv2.1, upregulated survivin, endothelial dysfunction and hyperresponsiveness to 5-HT were unaffected by quercetin. Quercetin significantly restored the decrease in Kv currents, the upregulation of 5-HT2A receptors and reduced the Akt and S6 phosphorylation. In vitro, quercetin induced pulmonary artery vasodilator effects, inhibited pulmonary artery smooth muscle cell proliferation and induced apoptosis. In conclusion, quercetin is partially protective in this rat model of PAH. It delayed mortality by lowering PAP, RVH and vascular remodeling. Quercetin exerted effective vasodilator effects in isolated PA, inhibited cell proliferation and induced apoptosis in PASMCs. These effects were associated with decreased 5-HT2A receptor expression and Akt and S6 phosphorylation and partially restored Kv currents. Therefore, quercetin could be useful in the treatment of PAH.es_ES
dc.description.sponsorshipThis work was supported by grants and fellowships by the Spanish Ministerio de Economia y Competitividad (SAF2011-28150 to F.P-V, SAF2010-22066-C02-01 to JD, and −02 to AC); Instituto de Salud Carlos III Red HERACLES RD06/0009 to JD; Miguel Servet Program CP12/03304 to LM; predoctoral grants BES-2012-051904 to DMS, CM, JMS, and PG; and Junta de Andalucia (Proyecto de excelencia, P12-CTS-2722).es_ES
dc.language.isoenges_ES
dc.publisherPublic Library of Science (PLOS)es_ES
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivs 3.0 Licensees_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es_ES
dc.subjectPulmonary arterieses_ES
dc.subjectBlood pressurees_ES
dc.subjectPulmonary hypertensiones_ES
dc.subjectCell membranes es_ES
dc.subjectVasodilators es_ES
dc.subjectApoptosises_ES
dc.subjectMembrane potentiales_ES
dc.subjectMembrane staininges_ES
dc.titleThe Flavonoid Quercetin Reverses Pulmonary Hypertension in Ratses_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES
dc.identifier.doi10.1371/journal.pone.0114492


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