Trimetazidine ameliorates myocardial ischemia-reperfusion injury

Aim of this study was to investigate the effects of trimetazidine attenuating the myocardial ischemiareperfusion injury to myocardium in rats and the underlying mechanisms. A model of myocardial ischemia reperfusion was established via ligating the left anterior descending coronary artery in 30 rats, and then they were randomly assigned to model group (n=10), low dose group (n=10) and high dose group (n=10). Moreover, additional 10 rats were collected and allocated to sham operation group, which was served as control group. Then, rats in the low dose group and high dose group were given trimetazidine with the dose of 10mg/kg and 30mg/kg respectively by intragastric administration, while rats in the control group and model group were given the equivalent volume saline. The dose was given once a day for consecutive 4 weeks in all rats. Echocardiography was applied to evaluate cardiac function, including left ventricular end-systolic dimension (LVESD), left ventricular end diastolic dimension (LVEDD) and left ventricular ejection fraction (LVEF). Next, myocardial tissue was collected, and Bax and Bcl-2 mRNA and the protein levels in the four groups were detected by RT-PCR and Western blot respectively. The level of malonaldehyde (MDA) and super oxide dismutase (SOD) activity in rat myocaridum in each group were detected by colorimetric methods, while the variables of apoptosis were measured by TUNEL methods. In comparison with the control group, LVEDD, LVEDS of rats increased significantly, LVEF decreased obviously, as well as Bax level, MDA level and the apoptotic variables in myocardial tissue increased (P<0.05), but Bc1-2 level and SOD activity decreased significantly in low dose, high dose and model group (P<0.05). Compared with model group, LVEDD, LVEDS of rats decreased obviously, LVEF increased significantly, as well as Bax level, MDA level and the apoptotic variables in myocardial tissue decreased (P<0.05), but Bcl-2 level and SOD activity increased significantly in low dose group, high dose group (P<0.05). The regulatory role of trimetazidine on above indicators of rats was in a dose-dependent manner. Conclusion: Trimetazidine can ameliorate rat myocardium following ischemia-reperfusion injury by effectively attenuating the injury from myocardial cell apoptosis; meanwhile, it can resist cell apoptosis through regulating Bax and bcl-2 expression, which exhibits guiding significance for the treatment of myocardial ischemia and reperfusion.