Effect of trimetazidine preconditioning on ischemia-reperfusion injury of rat cardiomyocyte apoptosis and expression of Mn-superoxide dismutase

Objective To investigate the effect protection of trimetazidine pretreatment on myocardial ischemia-reperfusion injury (MIRI) in rats and its mechanism. Methods Thirty health male Sprague-Dawley rats were randomly divided into three groups, Sham group (group A), ischemia-reperfusion group (group B), trimetazidine preconditioning groups (group C). Hematoxylin-eosinstaining (HE) method was used to identify the myocardial tissue. DNA in situ end labeling (TUNEL) was used to detected the apoptosis of cardiomyocytes. The serum levels of creatine kinase (CK), creatine kinase isoenzyme MB (CK-MB), superoxide dismutase (SOD), malondialdehyde (MDA) were measured and the expression of mRNA level of B cell lymphoma/leukemia-2 (bcl-2), bcl-2 associated X protein (bax) and cysteinyl aspartate-specific protease (Caspase)-3 were measured by the method of reverse transcription polymerase chain reaction (RT-PCR). Statisticalanalysis of data using the statistical product and service solutions 19.0 software. Results Compared with the group A, group B and C were present clear myocardial ischemia and myocardial infarction area. In group B, the myocardial cells were severely edematous and the fibers were disordered. In group C, the swelling myocardial cells were alleviated and the apoptosis rate of cardiomyocytes was significantly decreased (F=509.000, P<0.01). Compared with the group B, the activity of SOD (84.21±6.07) μg/L and the expression of bcl-2 at the mRNA level (3.12±1.86)in group C were increased (t=15.399, 16.141, P<0.01). The content of MDA, CK, CK-MB (33.58±3.73) mmol/L, (177.93±5.11) U/L, (50.92±2.94) U/L and The level of bax, Caspase-3 at the mRNA level in group C (2.41±0.19, 2.34±0.23) were significantly decreased (t=13.563, 24.944, 13.375, 31.696, 19.004, P<0.01). Conclusion Trimetazidine pretreatment can significantly decreases the apoptosis of myocardium induced by MIRI, could protect the myocardium of rats from ischemic reperfusion injury. Key words: Trimetazidine; Myocardial ischemia; Reperfusion injury; Apoptosis