Utilize este identificador para referenciar este registo: https://hdl.handle.net/10316/109913
Título: Protective role of malvidin-3-glucoside on peroxynitrite-induced damage in endothelial cells by counteracting reactive species formation and apoptotic mitochondrial pathway
Autor: Paixão, Joana Isabel Félix 
Dinis, Teresa C. P. 
Almeida, Leonor
Data: 2012
Editora: Hindawi
Projeto: PTDC/SAU-OSM/ 102907/2008 
SFRH/ BD/31568/2006 
Título da revista, periódico, livro ou evento: Oxidative Medicine and Cellular Longevity
Volume: 2012
Resumo: 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.
URI: http://hdl.handle.net/10316/109913
ISSN: 1942-0900
1942-0994
DOI: 10.1155/2012/428538
Direitos: openAccess
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