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Protective Role of Malvidin-3-Glucoside on Peroxynitrite-Induced Damage in Endothelial Cells by Counteracting Reactive Species Formation and Apoptotic Mitochondrial Pathway

The 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 apo...

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Autores principales: Paixão, Joana, Dinis, Teresa C. P., Almeida, Leonor M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3388314/
https://www.ncbi.nlm.nih.gov/pubmed/22792413
http://dx.doi.org/10.1155/2012/428538
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author Paixão, Joana
Dinis, Teresa C. P.
Almeida, Leonor M.
author_facet Paixão, Joana
Dinis, Teresa C. P.
Almeida, Leonor M.
author_sort Paixão, Joana
collection PubMed
description The 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.
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spelling pubmed-33883142012-07-12 Protective Role of Malvidin-3-Glucoside on Peroxynitrite-Induced Damage in Endothelial Cells by Counteracting Reactive Species Formation and Apoptotic Mitochondrial Pathway Paixão, Joana Dinis, Teresa C. P. Almeida, Leonor M. Oxid Med Cell Longev Research Article The 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. Hindawi Publishing Corporation 2012 2012-06-20 /pmc/articles/PMC3388314/ /pubmed/22792413 http://dx.doi.org/10.1155/2012/428538 Text en Copyright © 2012 Joana Paixão et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Paixão, Joana
Dinis, Teresa C. P.
Almeida, Leonor M.
Protective Role of Malvidin-3-Glucoside on Peroxynitrite-Induced Damage in Endothelial Cells by Counteracting Reactive Species Formation and Apoptotic Mitochondrial Pathway
title Protective Role of Malvidin-3-Glucoside on Peroxynitrite-Induced Damage in Endothelial Cells by Counteracting Reactive Species Formation and Apoptotic Mitochondrial Pathway
title_full Protective Role of Malvidin-3-Glucoside on Peroxynitrite-Induced Damage in Endothelial Cells by Counteracting Reactive Species Formation and Apoptotic Mitochondrial Pathway
title_fullStr Protective Role of Malvidin-3-Glucoside on Peroxynitrite-Induced Damage in Endothelial Cells by Counteracting Reactive Species Formation and Apoptotic Mitochondrial Pathway
title_full_unstemmed Protective Role of Malvidin-3-Glucoside on Peroxynitrite-Induced Damage in Endothelial Cells by Counteracting Reactive Species Formation and Apoptotic Mitochondrial Pathway
title_short Protective Role of Malvidin-3-Glucoside on Peroxynitrite-Induced Damage in Endothelial Cells by Counteracting Reactive Species Formation and Apoptotic Mitochondrial Pathway
title_sort protective role of malvidin-3-glucoside on peroxynitrite-induced damage in endothelial cells by counteracting reactive species formation and apoptotic mitochondrial pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3388314/
https://www.ncbi.nlm.nih.gov/pubmed/22792413
http://dx.doi.org/10.1155/2012/428538
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