6533b829fe1ef96bd1289b71

RESEARCH PRODUCT

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

Susana M. MoscaJuliana Catalina FantinelliJosé Luis RíosLuisa Fernanda González ArbeláezClaudia I. CaldizAlejandro Ciocci PardoGuillermo Raúl Schinella

subject

Male0301 basic medicineMyocardial InfarctionWistarBlood Pressure030204 cardiovascular system & hematologyPharmacologyMitochondrial Membrane Transport ProteinsInfarct sizeSHRGlycogen Synthase Kinase 3chemistry.chemical_compound0302 clinical medicineMITOCHONDRIAIschemiaSuperoxidesEnosRats Inbred SHRbiologySuperoxideMPTPINFARCT SIZEHeart//purl.org/becyt/ford/3.1 [https]GlutathioneMitochondriaMedicina BásicaHypertension//purl.org/becyt/ford/3 [https]General Agricultural and Biological SciencesPerfusionCocaCardiotonic AgentsCIENCIAS MÉDICAS Y DE LA SALUDInmunologíaIschemiaIn Vitro Techniques03 medical and health sciencesPOLYPHENOLSWISTARmedicineAnimalsHumansRats WistarSHR; Wistar; infarct size; mitochondria; polyphenolsMitochondrial Permeability Transition PorePlant ExtractsMyocardiumCocoa ExtractPolyphenolsGeneral ChemistryGlutathionemedicine.diseasebiology.organism_classificationRats030104 developmental biologychemistryMitochondrial permeability transition poreCiencias Médicas

description

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.

https://doi.org/10.1021/acs.jafc.6b01669