Effect of naloxone on expression of Bcl-2 protein and tumor necrosis factor-α in rats with acute myocardial ischemia/reperfusion injury

ObjectiveTo investigate the effect of naloxone on myocardial cell apoptosis and apoptosis- related gene Bcl-2 in rats with acute myocardial ischemia/ reperfusion (AMIR) injury, and explore the mechanism of protective effect of naloxone on myocardium. Methods Thirty SD rats were randomly divided into three groups (n=10): ischemia/reperfusion group, naloxone preconditioning group (naloxone was injected intraperitoneally 10 minutes before ischemia and 2 hours after reperfusion), and normal control group. The left anterior descending branch (LAD) of rat coronary artery was tied and untied in ischemia/reperfusion group and naloxone preconditioning group to establish the AMIR model in rats. The animals were then sacrificed and hearts were harvested .The expression of Bcl-2 protein was observed by immunohistochemical technique. Radioimmunoassay (RIA) was used to determine tumor necrosis factor -α (TNF-α) in serum. Results In the normal control group, there was no Bcl-2 expression and TNF-α level was (0.39±0.06)μg/L. Higher expression of Bcl-2 and increased TNF-α levels were found in ischemia/reperfusion group. The expression of Bcl-2 protein increased significantly 〔(+++) vs.(+)〕, and TNF-α was significantly lower in naloxone preconditioning group than those in the normal control group 〔(0.55±0.12)μg/L vs. (0.86±0.11)μg/L,P0.01〕. Conclusion Naloxone can protect myocardium from AMIR injury by inhibiting the apoptosis of cardiomyocytes induced by TNF-α and up-regulating protein expression of bcl-2 gene.