Objective:To investigate the effects of Urocortin-postconditioning on mitochondria-dependentapoptotic pathway.Methods: 24 Wistar rats were randomly divided into 3 groups(n=8):Control group(CON)

I/R group(I/R)

Urocortin group(UCN).The left ventricular samples in the Control group were collected as pre-ischemia controls through thoracotomy.After isolated heart Langendoff and Neely models were established

the rat hearts in the I/R group and the UCN group were continuously perfused with Krebs-Henseleit (K-H)buffersolution for 30 min

then the rat hearts were arrested by cardioplegia

St.Thomas-2 solution(STH-2)for 30min.After that

the rat hearts in the I/R group were reperfused with K-H buffer solution for 90 min.The rat hearts in the UCN group were reperfused with K-H buffer solution containing 10-8 mol/L Urocortin for 90 min.The releasing of Cyto C protein into cytosol was detected by Western blot.The expression of Caspase-3 protein in cardiomyocyte was detected by immunohistochemical assay.The apoptosis index (AI)of cardiomyocyte was detected by TUNEL.Results:Compared with Control group

the expression ofCaspase-3 and Cyto Cprotein in the I/R group and the UCN group were significantly increased(P<0.05).Caspase-3 and Cyto C protein in the UCN group were lowly expressed than those in the I/R group(0.24±0.70 vs 0.36±0.15

P<0.05

0.88±0.07 vs 1.29±0.02

P<0.05).After reperfusion

apoptosis index(AI)in the I/R group and UCN group were significantly higher than that in the Control group(P<0.05);Compared with I/R group group

AI in UCN group was decreased increased(6.77±1.12 vs 12.81±0.62

P<0.05).The expression of Caspase-3 protein had a positive correlation with Cyto C protein in cytosol(r=0.775

P<0.05)

and the apoptosis index(AI)of cardiomyocyte had a positive correlation with Cyto Cprotein in cytosol(r=0.865

P<0.05)。Conclusion:Urocortin protect hearts from ischemic-reperfusion injury through interfering mitochondria-dependent apoptotic pathway.