| ObjectiveTo investigate the effects of sevoflurane preconditioning-induced delayed protection on cardiomyocyte apoptosis in rats with myocardial ischemia/reperfusion (I/R) injury.MethodsAdult male Sprague Dawley (SD) rats, weighing 270～350 g, 63 in total, were used in-vivo study. The rats were randomly divided into four groups: (1) Sham group: the rats received 33% oxygen for 2 h only without subsequent I/R; (2) I/R group: the rats were assigned to receive 33% oxygen for 2 h. 24 h later, the rats were subjected to coronary artery occlusion for 30 min followed by reperfusion for 2 h; (3) SEVO group: the rats received 2.5% sevoflurane only without I/R. Triphenyl tetrazolium chloride (TTC) staining was used to measure the myocardial infarct size; (4) SWOP group: the rats received 2.5% sevoflurance for 2 h on the first day and were subjected to I/R after 24 hrs. TUNEL assary was used to evluate the myocardial apoptosis. Western blot analysis was applied in determining the expression levels of apoptosis with caspase recruitment domain (ARC) and active Caspase-8 in the left ventricules.ResultsSevoflurane preconditioning significantly decreased the infarct size and the myocardium apoptosis in rats subjected to I/R injury(P<0.05). SWOP already induced an marked up-regulation of ARC protein expression in heart before ischemia (P<0.05); and also alleviated the down regualtion of ARC expression induced by ischemia/reperfusion at the end of reperfusion. Moreover, active Caspase-8 were significantly increased in the I/R group. But this was significantly attenuated by Sevoflurane preconditioning (P<0.05). ConclusionSevoflurane preconditioning-induced delayed protection attenuates ischemia / reperfusion injury through up-regulating the anti-apoptosis protein ARC expression, which in turn inhibited Caspase-8 expression and eventually reduced the myocardial apoptosis index and the myocardial infarct size in rats. |
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