Effects Of Sufentanil Postconditioning On Myocardial Ischemia-Reperfusion Injury In Dogs And Its Relationship To The JAK2-STAT3 Signaling Pathway

Objective To investigate the anti-apoptotic effects of sufentanil postconditioning on myocard ialischemia-reperfusion injury and its relationship to the JAK2-STAT3 signaling pathway.Methods Twenty- four dogs were randomly divided into 4 groups:sham group (sham–operation),I/Rgroup(ischemia-reperfusion),SPOgroup (sufentanil postconditioning+I/R,),SPO+AG490group(AG490+sufentanil postconditioning+I/R,),except that sham group,all dogs subjected to 30min of myocardial ischemia followed by 120 min of reperfusion.After reperfusion two hours ,thepresence of apoptosis was determined quantitavely by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) methods,immunohistochemistry was used to detectthe Bcl-2 and Bax protein of myocardial tissue.Results In light-microscopy , the myocardial tissue of the I/R group was significantly impaired,the pathological lesion were lighter in SPO group than in I/R group significantly(P<0.05);Asignificant number of TUNEL positive cells [(63.9±3.987)%] were observed in myocardialtissue from hearts subjected to 30 min of myocardial ischemia fo llowed by 120 min ofreperfusion. Administration of sufentanil exerted a significant anti-apoptotic effect, as evidencedby reduced TUNEL-positive staining [(30.7±1.515)%]; compared with the group Sham,expression of Bcl-2 and Bax is increased in myocardial group I/R, group SPO and groupSPO+AG490. Bcl-2/Bax ratio is lower in group I/R and higher in group SPO; P-STAT3 activitywas increased in the myocardial tissue after sufentanil postconditioning compared with that ingroup Sham(P<0.05).Conclusion Myocardial ischemia-reperfusion injury may induce cell apoptosis, and sufentanilpostconditioning have certain inhibition of cell apoptosis, and via the activation JAK2-STAT3signal transduction pathways up-regulation of Bcl-2 expression and down-regulation Baxexpression to paly a role.