EFFECT OF ILEX PARAGUARIENSIS (YERBA MATE) EXTRACT ON INFARCT SIZE IN ISOLATED RAT HEART: MECHANISMS INVOLVED

GONZÁLEZ ARBELÁEZ LF; FANTINELLI JC; FANTINELLI JC; CIOCCI PARDO, A; CALDIZ, CI; RIOS J; SCHINELLA GR; MOSCA SM

Food & Function - Royal Society of Chemistry

Royal Society of Chemistry

Lugar: Washington DC; Año: 2015

2042-6496

Ilex paraguariensis (IP) dried and minced leaves made into a brewed tea are a beveragewidely consumed by large populations in South America as a source of caffeine (stimulantaction) and for its medicinal properties. However, there is little information about the actionsof IP on myocardium in ischemia-reperfusion situation. Therefore, the objective of this studywas to examine the effects of an aqueous extract of IP on infarct size in a model of regionalischemia. Isolated rat hearts were perfused by Langendorff technique and submitted to 40-minof coronary artery occlusion followed by 60 min of reperfusion (ischemic control hearts).Other hearts received IP 30 μg/mL during the first 10 min of reperfusion in absence orpresence of LG-nitro-L-arginine methyl ester [L-NAME, a nitric oxide synthase (NOS)inhibitor]. Infarct size was determined by triphenyltetrazolium chloride (TTC) staining.Postischemic myocardial function and coronary perfusion were also assessed. Cardiacoxidative damage was evaluated by the thiobarbituric acid reactive substances (TBARS)concentration and reduced glutathione (GSH) content. To analyze the mechanisms involvedthe expression of phosphorylated forms of eNOS and Akt were measured. In isolatedmitochondria the Ca2+-induced mitochondrial permeability transition pore (mPTP) openingwas determined. IP significantly decreased the infarct size and improved postischemicmyocardial function and coronary perfusion. TBARS decreased, GSH was partiallypreserved, levels of P-eNOS and P-Akt increased and mPTP opening diminished after IPaddition. These changes were abolished by L-NAME. Therefore, our data demonstrate thatthe acute treatment with IP only during reperfusion was effective to reduce myocardialpostischemic alterations. These actions would be mediated by a decrease of mitochondrialpermeability through IP-activated Akt/eNOS-dependent pathways.