Effect of sufentanil postconditioning on level of cathepsin B in myocardium during ischemia-reperfusion in rats

Objective To evaluate the effect of sufentanil postconditioning on the level of cathepsin B in the myocardium during ischemia-reperfusion(I/R)in the rats. Methods Eighteen healthy adult male Sprague-Dawley rats, weighing 250-300 g, were divided into 3 groups(n=6 each)using a random number table: sham operation group(group S), group I/R and sufentanil postconditioning group(group SP). The rats were anesthetized with intraperitoneal 20% urethane 5 ml/kg.Myocardial I/R was induced by occlusion of the left anterior descending branch of the coronary artery for 30 min followed by 120 min reperfusion.At 5 min before reperfusion, sufentanil 1.0 μg/kg was intravenously injected in group SP, and the equal volume of normal saline was given instead in S and I/R groups.At the end of reperfusion, blood samples from the abdominal aorta were collected for determination of serum cardiac troponin I(cTnI)and creatine kinase-MB(CK-MB)concentrations, and myocardial specimens were obtained for examination of the ultrastructure of cardiomyocytes(using transmission electron microscopy)and for determination of Beclin-1, microtubule-associated protein 1 light chain 3Ⅱ(LC3Ⅱ)and cathepsin B expression(by Western blot)and cathepsin B activity(by fluorometric assay). Results Compared with group S, the serum cTnI and CK-MB concentrations were significantly increased, the expression of Beclin-1, LC3Ⅱ and cathepsin B was up-regulated, and the activity of cathepsin B was enhanced in I/R and SP groups(P<0.05). Compared with group I/R, the serum cTnI and CK-MB concentrations were significantly decreased, the expression of Beclin-1 and LC3Ⅱ was down-regulated, the expression of cathepsin B was up-regulated, and the activity of cathepsin B was enhanced(P<0.05), the pathological changes of myocardial tissues were significantly attenuated, and autophagosomes were reduced in group SP. Conclusion The mechanism by which sufentanil postconditioning inhibits cardiomyocyte autophagy during myocardial I/R is probably related to increased expression and activity of cathepsin B in rats. Key words: Sufentanil; Cathepsin B; Myocardial reperfusion injury; Ischemic postconditioning