Objective: To study the protective effect of 17-methoxyl-7-hydroxyl-benzofuran chalcone (YLSC) postconditioning on myocardial ischemia reperfusion (I/R) injury in isolated rat hearts and investigate its related signaling pathway. Method: Total 60 male SD rats were randomly divided into 5 groups:normal group

model group

YLSC group (5 μmol·L-1)

AG490 group (2 μmol·L-1) and YLSC+inhibitor group (YLSC 5 μmol·L-1+AG490 2 μmol·L-1)

n=12 in each group. The isolated rat hearts were subjected to 30 min ischemia+120 min reperfusion to establish the I/R model. AG490 or YLSC was given 10 min before reperfusion. The heart rate (HR)

the left ventricular end diastolic pressure (LVEDP) and the maximum change rate of left ventricular pressure (±dp/dtmax) were recorded

and the level of lactic dehydrogenase (LDH) in coronary effluent was detected. The rats were sacrificed after reperfusion

and their infarct sizes were measured by triphenyltetrazolium chloride(TTC) staining. Phosphorylated janus kinase 2 (JAK2)

phosphorylated signal transducer and activator of transcription 3 (STAT3)

B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) protein expression levels in myocardium were measured by Western blot. Result: As compared with the model group

YLSC postconditioning obviously ameliorated cardiac function

decreased myocardial infarct sizes and LDH level

reduced apoptotic rate and Bax expression levels

and increased p-JAK2

p-STAT3 and Bcl-2 levels (P<0.05

P<0.01). Combination of YLSC and AG490 could attenuate the hemodynamic improvement effect

increase the infarct sizes

LDH level and Bax expression level

and down-regulate p-JAK2

p-STAT3 and Bcl-2 expression levels as compared with YLSC group (P<0.05

P<0.01). Conclusion: YLSC postconditioning could effectively protect against myocardial I/R injury in isolated rat hearts

and its mechanism may be associated with activation of JAK2/STAT3 signaling pathway.