Abstract: OBJECTIVE To investigate the protective effect of sulforaphane on cardiac myocyte injured by ischemia-reperfusion injury(IRI) and study the possible mechanism. METHODS Cardiac myocytes from neonatal SD rats were cultured and pretreated with low-, medium-, high-concentration(10, 20, 40 μg·ml^-1) of sulforaphane and JAK2 inhibitor (SAR302503), before exposure to hypoxia (95%N₂-5%CO₂) for 24 h and reoxygenation (95% air-5%CO₂) for 1 h to create cell model of ischemia-reperfusion. CCK8 kit was used to observe the effect of sulforaphane on the relative survival rate of cardiac myocyte. Related kits were used to analyze the lactate dehydrogenase (LDH) level, methylenediox yamphetamine (MDA) level and superoxide dismutase (SOD) activity. Western blot was used to determine the levels of the related proteins in JAK2/STAT3 signaling pathway. RESULTS Compared with control group, the relative survival rate of cardiac myocyte in IRI group was significantly decreased (P<0.05), the LDH and MDA levels in IRI group highly increased (P<0.05), SOD activity sharply decreased (P<0.05), the expression levels of p-JAK2 and p-STAT3 in IRI group were significantly increased (P<0.05). As compared with IRI group, the relative survival rate of cardiac myocyte in sulforaphane and inhibitor groups were significantly increased(P<0.05), the LDH and MDA levels in sulforaphane and inhibitor groups highly decreased(P<0.05), SOD activity sharply increased(P<0.05), the expression levels of p-JAK2 and p-STAT3 in sulforaphane and inhibitor groups were significantly decreased(P<0.05). CONCLUSION Sulforaphane has a protective effect on cardiac myocyte injured by ischemia-reperfusion, which is partially via suppressing the activation of JAK2/STAT3 signaling pathway.