Protective effects of N-(2-mercaptopropionyl)-glycine against ischemia–reperfusion injury in hypertrophied hearts

• Published in: Experimental and molecular pathology 2013-02, Vol.94 (1), p.277-284
• Main Authors: Fantinelli, Juliana C., González Arbeláez, Luisa F., Pérez Núñez, Ignacio A., Mosca, Susana M.
• Format: Article
• Language: English
• Subjects: Animals; Blood Pressure - drug effects; Cardiotonic Agents - pharmacology; Glutathione - analysis; Glycine - analogs & derivatives; Glycine - pharmacology; GSH; Hypertension - complications; Hypertrophy, Left Ventricular - complications; Male; Mitochondrial Membrane Transport Proteins - metabolism; MPG; mPTP; Myocardial infarction; Myocardial Reperfusion Injury - complications; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - prevention & control; Myocardium - pathology; Oxidative Stress; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Reactive Oxygen Species - metabolism; SHR; SOD; Sulfhydryl Compounds - pharmacology; Superoxide Dismutase - metabolism; Thiobarbituric Acid Reactive Substances - analysis; WKY
• ISSN: 0014-4800; 1096-0945
• DOI: 10.1016/j.yexmp.2012.07.004

The beneficial effects of N-(2-mercaptopropionyl)-glycine (MPG) against ischemia–reperfusion injury in normotensive animals have been previously studied. Our objective was to test the action of MPG during ischemia and reperfusion in hearts from spontaneously hypertensive rats (SHR). Isolated hearts from SHR and age-matched normotensive rats Wistar Kyoto (WKY) were subjected to 50-min global ischemia (GI) and 2-hour reperfusion (R). In other hearts MPG 2mM was administered during 10min before GI and the first 10min of R. Infarct size (IS) was assessed by TTC staining technique and expressed as percentage of risk area. Postischemic recovery of myocardial function was assessed. Reduced glutathione (GSH), thiobarbituric acid reactive substances (TBARS) and SOD cytosolic activity — as estimators of oxidative stress and MnSOD cytosolic activity — as an index of (mPTP) opening were determined. In isolated mitochondria H2O2-induced mPTP opening was also measured. The treatment with MPG decreased infarct size, preserved GSH levels and decreased SOD and MnSOD cytosolic activities, TBARS concentration, and H2O2 induced-mPTP opening in both rat strains. Our results show that in both hypertrophied and normal hearts an attenuation of mPTP opening via reduction of oxidative stress appears to be the predominant mechanism involved in the cardioprotection against reperfusion injury MPG-mediated. ► We examine the effects of MPG on reperfusion injury in SHR. ► We demonstrate the participation of mitochondrial pore. ► We establish the effects associated to oxidative stress.