Objective:To investigate the effect of JAK2/STAT3 pathway on myocardial protection of tetrodotoxin(TTX) cardioplegia in rat hearts.Methods:A total of 24 Wistar rats were randomly divided into Group Control

Group TTX and Group TTX+AG490(n=8).The left ventricular samples in Group Control were collected as pre-ischemia control through thoracotomy.After isolated heart Langendorff and Neely models were established

the rat hearts in Group TTX were continuously perfused with Krebs-Henseleit(K-H) buffer solution for 30 minutes

arrested by TTX cardioplegia(4℃) for 60 minutes

and underwent reperfusion with K-H buffer solution for 60 minutes

then the left ventricular samples were collected for detections.The rat hearts in Group TTX+AG490 were perfused and reperfused with JAK2 inhibitor AG490(5μmol/L) and K-H buffer solution under the same procedure as Group TTX.The protein expression indexes(PEI) of phosphorylated-STAT3(p-STAT3) and B-cell lymphoma-2(Bcl-2) in myocardium were detected by immunohistochemical assay(IHC).The apoptosis index(AI) of cardiomyocyte was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL).The changes of these indexes in three groups were used for comparison.Results:Compared with Group Control

the PEI of p-STAT3 and Bcl-2 in Group TTX and Group TTX+AG490 increased significantly(P<0.05);Treated with AG490

the PEI of p-STAT3 and Bcl-2 in Group TTX+AG490 was lower than that in Group TTX(P<0.05).The PEI of Bcl-2 had a positive correlation with the PEI of p-STAT3(r=0.743

P<0.05).After ischemia/reperfusion

AI in Group TTX and Group TTX+AG490 were significantly higher than that in Group Control(P<0.05);compared with Group TTX

AI in Group TTX+AG490 increased significantly(P<0.05).Conclutions:JAK2/STAT3 pathway could mediate myocardial protection of TTX cardioplegia in rat hearts via upregulating the protein expression of Bcl-2 and suppressing cardiomyocytes apoptosis.