Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/109913
DC FieldValueLanguage
dc.contributor.authorPaixão, Joana Isabel Félix-
dc.contributor.authorDinis, Teresa C. P.-
dc.contributor.authorAlmeida, Leonor-
dc.date.accessioned2023-11-06T12:41:55Z-
dc.date.available2023-11-06T12:41:55Z-
dc.date.issued2012-
dc.identifier.issn1942-0900pt
dc.identifier.issn1942-0994pt
dc.identifier.urihttp://hdl.handle.net/10316/109913-
dc.description.abstractThe health-promoted benefits of anthocyanins, including vascular protective effects and antiatherogenic properties, have now been recognized, but the involved molecular mechanisms have not been well elucidated. Following our previous work on cytoprotective mechanisms of some anthocyanins against apoptosis triggered by peroxynitrite in endothelial cells, here we investigated the protective role of malvidin-3-glucoside, a major dietary anthocyanin, on such deleterious process, by exploring the interference on cellular reactive species formation and on apoptotic mitochondrial pathway. Preincubation of cells with 25 μM malvidin-3-glucoside protected efficiently endothelial cells from peroxynitrite-promoted apoptotic death, an effect which may be partially mediated by its ability to decrease the formation of reactive species after cell aggression, as assessed by the dichlorodihydrofluorescein diacetate assay and by carbonyl groups formation. Moreover, malvidin-3-glucoside inhibited mitochondrial apoptotic signaling pathways induced by peroxynitrite, by counteracting mitochondrial membrane depolarization, the activation of caspase-3 and -9, and the increase in the expression of the proapoptotic Bax protein. Altogether, our data expands our knowledge about the molecular mechanisms underlying the vascular protection afforded by malvidin-3-glucoside, and anthocyanins in general, in the context of prevention of endothelial dysfunction and atherosclerosis.pt
dc.language.isoengpt
dc.publisherHindawipt
dc.relationPTDC/SAU-OSM/ 102907/2008pt
dc.relationSFRH/ BD/31568/2006pt
dc.rightsopenAccesspt
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt
dc.subject.meshAnimalspt
dc.subject.meshAnthocyaninspt
dc.subject.meshAortapt
dc.subject.meshApoptosispt
dc.subject.meshCaspase 3pt
dc.subject.meshCaspase 9pt
dc.subject.meshCattlept
dc.subject.meshCell Survivalpt
dc.subject.meshCytoplasmpt
dc.subject.meshCytoprotectionpt
dc.subject.meshEndothelial Cellspt
dc.subject.meshEnzyme Activationpt
dc.subject.meshFree Radical Scavengerspt
dc.subject.meshGlucosidespt
dc.subject.meshIntracellular Spacept
dc.subject.meshMembrane Potential, Mitochondrialpt
dc.subject.meshMitochondriapt
dc.subject.meshOxidation-Reductionpt
dc.subject.meshPeroxynitrous Acidpt
dc.subject.meshProtective Agentspt
dc.subject.meshReactive Oxygen Speciespt
dc.subject.meshRhodaminespt
dc.subject.meshSignal Transductionpt
dc.subject.meshbcl-2-Associated X Proteinpt
dc.titleProtective role of malvidin-3-glucoside on peroxynitrite-induced damage in endothelial cells by counteracting reactive species formation and apoptotic mitochondrial pathwaypt
dc.typearticle-
degois.publication.firstPage428538pt
degois.publication.lastPage12pt
degois.publication.titleOxidative Medicine and Cellular Longevitypt
dc.peerreviewedyespt
dc.identifier.doi10.1155/2012/428538pt
degois.publication.volume2012pt
dc.date.embargo2012-01-01*
uc.date.periodoEmbargo0pt
item.grantfulltextopen-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.openairetypearticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextCom Texto completo-
crisitem.author.researchunitCNC - Center for Neuroscience and Cell Biology-
crisitem.author.orcid0000-0001-6350-5741-
Appears in Collections:FFUC- Artigos em Revistas Internacionais
I&D CNC - Artigos em Revistas Internacionais
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