EGCG decreases myocardial infarction in both I/R and MIRI rats through reducing intracellular Ca2+ and increasing TnT levels in cardiomyocytes

Background.Myocardial ischemia/reperfusion injury (MIRI) usually induces serious health problems.Objectives.This study attempted to explore protective effects of (-)-epigallocatechin-3-gallate (EGCG) on MIRI and the associated mechanism. Materials and methods.Ischemia/reperfusion of an isolated rat heart (I/R model) and the MIRI model were used in this study.Myocardial infarction was measured with staining with 2,3,5-triphenyltetrazolium chloride (TTC).Ca 2+ and troponin T (TnT) concentrations in coronary perfusion fluid were evaluated using the chromatometry method.Ca 2+ concentration in cardiomyocytes was determined with detecting Ca 2+ fluorescence intensity.The ultrastructure of cardiomyocytes was observed using transmission electron microscopy (TEM).β-nicotinamide adenine dinucleotide (NAD + ) of cardiomyocytes was also determined. Results.The EGCG (I/R+EGCG) significantly reduced myocardial infarction size of isolated rat heart compared to I/R rats (p < 0.05), remarkably increased Ca 2+ and decreased TnT concentrations in coronary perfusion fluid of I/R rats compared to the I/R model (p < 0.05), as well as markedly decreased intracellular Ca 2+ concentration and promoted NAD + concentration in cardiomyocytes compared to I/R rats (p < 0.05).It also obviously maintained the mitochondrial structure in cardiomyocytes of I/R rats and improved the ultrastructure of cardiomyocytes of MIRI rats.Lonidamine (LND) treatment (I/R+EGCG+LND group) significantly blocked the effects of EGCG on I/R injury compared to the I/R+EGCG group (p < 0.05).The EGCG (MIRI+EGCG) significantly decreased myocardial infarction size compared to MIRI rats (p < 0.05) and remarkably enhanced Ca 2+ and reduced TnT concentrations in the pulmonary artery compared to that of MIRI rats (p < 0.05). Conclusions.The EGCG decreased myocardial infarction size in both I/R models and MIRI models by reducing intracellular Ca 2+ concentration, increasing TnT concentration, promoting NAD + concentration, and improving the ultrastructure of cardiomyocytes.