Acute treatment with copoazú fermented extract ameliorates myocardial ischemia-reperfusion injury via eNOS activation

•Copoazú fermented extract (CFE) protects against ischemia-reperfusion injury.•Fermentation decreases the antioxidant power and increases the cardioprotective efficacy.•Akt and PKCε-dependent pathways mediate the cardioprotection.•eNOS activation plays a crucial role in the attenuation of postischem...

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Published inJournal of functional foods Vol. 34; pp. 470 - 477
Main Authors Fantinelli, Juliana C., Cuéllar Álvarez, Liceth N., González Arbeláez, Luisa F., Ciocci Pardo, Alejandro, Galeano García, Paula L., Schinella, Guillermo R., Mosca, Susana M.
Format Journal Article
LanguageEnglish
Published Elsevier Ltd 01.07.2017
Elsevier
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Summary:•Copoazú fermented extract (CFE) protects against ischemia-reperfusion injury.•Fermentation decreases the antioxidant power and increases the cardioprotective efficacy.•Akt and PKCε-dependent pathways mediate the cardioprotection.•eNOS activation plays a crucial role in the attenuation of postischemic damage. Our aim was to examine the effects of aqueous extracts of fermented (CFE) and non-fermented (CNFE) ¨copoazú¨ (fruit of Theobroma grandiflorum) seeds against ischemia-reperfusion injury. Isolated rat hearts were submitted to 30min of global ischemia (GI) and 60min of reperfusion (R). Other hearts received CFE or CNFE in absence or in presence of L-NAME (a nitric oxide synthase inhibitor). Infarct size (IS) and post-ischemic myocardial function (PMF) were measured. Lipid peroxidation, reduced glutathione (GSH) and the expression of phosphorylated forms of eNOS, Akt, GSK-3β and PKCε were assessed. The response of isolated mitochondria to Ca2+ (MR) was also determined. CFE but not CNFE decreased IS, increased PMF and the expression of P-eNOS, P-Akt, P-GSK-3β and P-PKCε, partially preserved GSH and improved MR. These effects were lost in presence of L-NAME. These data demonstrate that the acute treatment with CFE protects the heart against ischemia-reperfusion damage through NOS-dependent mechanisms.
ISSN:1756-4646
2214-9414
DOI:10.1016/j.jff.2017.05.010