Abstract: AIM: To explore the protective effect and mechanism of schisandrin B (Sch B) on myocardial ischemia-reperfusion injury (MIRI) in rats.  METHODS: Forty SD rats were randomly divided into control group, MIRI group,MIRI+30 mg/kg Sch B (MIRI+L-Sch B) group and MIRI+60 mg/kg Sch B (MIRI+H-Sch B) group, ten in each group, Sch B were intragastrically for 7 days. Ligation of the left anterior descending branch was used to establish MIRI model, control group rats only underwent sham operation. The ardiac function parameters of ejection fraction (EF), fractional shortening (FS), maximum rate of increase in left ventricular pressure (+dp/dtmax), maximum rate of decline in left ventricular pressure (－dp/dtmax) values were recorded after 120 min reperfusion. CK-MB, LDH, cTnI activities in serum were detected. MPO, MDA and GSH-Px in myocardial tissue were detected. TTC, HE and TUNEL staining were used to detect myocardial infarction area, histopathological changes and cardiomyocyte apoptosis. Western blot was used to detect cleaved caspase 3, Bcl-2 and Bax protein in myocardial tissue. RESULTS: After Sch B pretreatment, the values of EF, FS, －dp/dtmax and levels GSH-PX in MIRI rats significantly increased (P<0.05 or P<0.01), while the activities of CK-MB, LDH, cTnI and MDA were significantly decreased (P<0.05 or P<0.01), myocardial infarction area significantly reduced (P<0.01), myocardial tissue damage was improved (P<0.01), cardiomyocyte apoptosis also reduced (P<0.05, P<0.01), cleaved caspase 3/caspase 3, Bax protein expression levels were significantly decreased (P<0.05 or P<0.01), Bcl-2 protein expression levels were significantly increased (P<0.05 or P<0.01); MIRI+H-Sch B group rats +dp The /dtmax value was significantly increased (P<0.05), and the MPO level was significantly decreased (P<0.01), shows dose-dependent effect.CONCLUSION: Pretreatment of Sch B attenuated MIRI-induced myocardial injury in rats, and its mechanism may related to inhibition oxidative stress, decreased cleaved caspase 3, Bax protein expression and increased Bcl-2 protein expression to inhibit cardiomyocyte apoptosis.

Key words: schisandrin B, myocardial ischemia reperfusion injury, oxidative stress, apoptosis