Effect of an Ilex paraguariensis (yerba mate) extract on infarct size in isolated rat hearts: the mechanisms involved

FANTINELLI JC; LF GONZÁLES ARBELAEZ; CIOCCI PARDO A; C CALDIZ; RIOS JL; SCHINELLA GR; MOSCA SM

Food and Function

Royal Society of Chemistry (Great Britain)

Lugar: Washington D.C; Año: 2016

Tea made from Ilex paraguariensis (IP) dried and minced leaves is a beverage widely consumed by largepopulations in South America as a source of caffeine (stimulant action) and for its medicinal properties.However, there is little information about the action of IP on the myocardium in the ischemia?reperfusioncondition. Therefore, the objective of this study was to examine the effects of an aqueous extract of IP oninfarct size in a model of regional ischemia. Isolated rat hearts were perfused by the Langendorff techniqueand subjected to 40 min of coronary artery occlusion followed by 60 min of reperfusion (ischemiccontrol hearts). Other hearts received IP 30 μg mL−1 during the first 10 min of reperfusion in the absenceor presence of LG-nitro-L-arginine methyl ester [L-NAME, a nitric oxide synthase (NOS) inhibitor]. Theinfarct size was determined by triphenyltetrazolium chloride (TTC) staining. Post-ischemic myocardialfunction and coronary perfusion were also assessed. Cardiac oxidative damage was evaluated by usingthe thiobarbituric acid reactive substance (TBARS) concentration and the reduced glutathione (GSH)content. To analyze the mechanisms involved, the expressions of phosphorylated forms of eNOS and Aktwere measured. In isolated mitochondria the Ca2± induced mitochondrial permeability transition pore(mPTP) opening was determined. IP significantly decreased the infarct size and improved post-ischemicmyocardial function and coronary perfusion. TBARS decreased, GSH was partially preserved, the levels ofP-eNOS and P-Akt increased and mPTP opening diminished after IP addition. These changes were abolishedby L-NAME. Therefore, our data demonstrate that acute treatment with IP only during reperfusionwas effective in reducing myocardial post-ischemic alterations. These actions would be mediated by adecrease of mitochondrial permeability through IP-activated Akt/eNOS-dependent pathways.