Objective To study the protective effect of schisandrin B on myocardial cells with hypoxia/reoxygenation-induced injury in neonatal rats,and observe its inhibitory role in endoplasmic reticulum stress.Methods Cardiac myocytes from neonatal SD rats were cultured and pretreated with schisandrin B with low-（10 mg/L）,medium-（100 mg/L）,high-（200 mg/L）concentration and SIRT1 inhibitor（Ex-527）,before exposure to hypoxia（95 %N2-5 %CO2）for 3 h and reoxygenation（95 % air-5 %CO,2,）for 3 h to create cell model of hypoxia/reoxygenation.The effect of schisandrin B on the relative survival rate of cardiac myocyte was detected.The lactate dehydrogenase（ LDH）level,methylenediox yamphetamine（MDA）level and superoxide dismutase（SOD）activity were investigated.Western Blot was used to determine the expression levels of GRP78,CHOP,Cleaved caspase12,SIRT1 and PGC-1α protein.Results Compared with the control group,the relative survive rate of cardiac myocyte in H/R group was significantly decreased（P ,<,0.05）,the LDH and MDA levels in I/R group were highly increased（P,<,0.05）,SOD activity was sharply decreased（P,<,0.05）,the expression levels of GRP78,CHOP,Cleaved caspase12 in I/R group were significantly increased（P,<,0.05）,and the expression levels of SIRT1 and PGC-1α were greatly decreased（P,<,0.05）.Compared with I/R group,the relative survival rate of cardiac myocyte in schisandrin B groups were significantly increased（P,<,0.05）,the LDH and MDA levels in schisandrin B groups highly were decreased（P,<,0.05）,SOD activity was sharply increased,the expression levels of GRP78,CHOP,Cleaved caspase12 in schisandrin B were significantly decreased（P,<,0.05）,and the expression levels of SIRT1 and PGC-1α were greatly increased（P,<,0.05）.However,the effect of Ex-527 on cardiac myocyte was opposite to schisandrin B.Conclusion Schisandrin B has a protective effect on cardiac myocyte injury caused by hypoxia/reoxygenation,which is partially via suppressing the endoplasmic reticulum stress.