Ex Vivo Treatment with a Polyphenol-Enriched Cocoa Extract Ameliorates Myocardial Infarct and Postischemic Mitochondrial Injury in Normotensive and Hypertensive Rats

Our objective was to determine the effects of a polyphenol-enriched cocoa extract (PCE) on myocardial postischemic alterations in normotensive (Wistar rats, W) and spontaneously hypertensive rats (SHR). Isolated hearts were submitted to 110 min of perfusion or 20 min stabilization, 30 min global isc...

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Detalles Bibliográficos
Autores: González Arbeláez, Luisa Fernanda, Ciocci Pardo, Alejandro, Fantinelli, Juliana Catalina, Caldiz, Claudia Irma, Ríos, José Luis, Schinella, Guillermo Raúl, Mosca, Susana Maria
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2016
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/53924
Acceso en línea:http://hdl.handle.net/11336/53924
Access Level:acceso abierto
Palabra clave:INFARCT SIZE
MITOCHONDRIA
POLYPHENOLS
SHR
WISTAR
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
Descripción
Sumario:Our objective was to determine the effects of a polyphenol-enriched cocoa extract (PCE) on myocardial postischemic alterations in normotensive (Wistar rats, W) and spontaneously hypertensive rats (SHR). Isolated hearts were submitted to 110 min of perfusion or 20 min stabilization, 30 min global ischemia, and 60 min reperfusion (R). Other hearts were treated with PCE at the onset of R. Infarct size, the reduced glutathione (GSH), and the expression of phospho-Akt, P-GSK-3β, and P-eNOS were assessed. In isolated mitochondria, the Ca2+-mediated response of mitochondrial permeability transition pore (mPTP), membrane potential (δψm), and superoxide production were determined. PCE decreased infarct size, partly preserved GSH, increased the P-Akt, P-GSK-3β, and P-eNOS contents, improved mPTP response to Ca2+, decreased the superoxide production, and restored δψm. These data show that PCE decreases the cardiac postischemic damage in W rats and SHR and suggest that Akt/GSK-3β/eNOS dependent pathways are involved.