Abstract : objective To investigate the anti-apoptotic effects of sufentanil postconditioning on myocardial ischemia-reperfusion injury and its relationship to the JAK2-STAT3 signaling pathway.methodsTwenty-four dogs were randomly divided into 4 groups : sham group (sham-operation),I/Rgroup(ischemia–reperfusion)SPOgroup(sufentanilpostconditioning+I/R ),SPO+AG490 group(AG490+sufentanil postconditioning+I/R,),except that sham group,all dogs subjected to 30 min of myocardial ischemia followed by 120 min of reperfusion.After reperfusion two hours ,the presence of apoptosis was determined quantitavely by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) methods,immunohistochemistry was used to detect the Bcl-2 、Bax p-STAT3 and protein of myocardial tissue.rexersults A significant number of TUNEL positive cells [(63.873±3.987)%] were observed in myocardial tissue from hearts subjected to 30 min of myocardial ischemia followed by 120 min of reperfusion.Administration of sufentanil exerted a significant anti-apoptotic effect,as evidenced by reduced TUNEL-positive staining [(30.737±1.515)%] ;compared with the sham group,expression of Bcl-2 and Bax is increased in myocardial ischemia reperfusion group, sufentani postconditining group and SPO + AG490 group.Bcl-2/Bax ratio is lower in I/R group and higher in SPO group; P-STAT3 activity was increased in the myocardial tissue after sufentanil postconditioning compared with that in sham-operation group(p<0.05).Conclusion sufentanil postconditioning provided myocardial protectiontoischemia–reperfusion injury on dogs,the mechanism of myocardial protection is related to the inhibition of cell apoptosis via up-regulation of Bcl-2 expression and down-regulation Bax expression.