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目的 探讨萝卜硫素对新生大鼠心肌细胞缺血再灌注损伤(ischemia-reperfusion injury, IRI)的保护效应,并对其作用机制进行初步研究.方法 体外培养新生大鼠心肌细胞于缺氧24 h复氧1 h构建IRI细胞模型,观察细胞损伤情况;并将低、中、高剂量萝卜硫素(10, 20, 40μg·mL-1)及JAK2抑制剂(SAR302503)分别加入培养基中,与细胞共同处理24h后,再置于上述缺氧复氧环境中培养,然后采用CCK8试剂盒检测萝卜硫素对心肌细胞增殖的影响,相关试剂盒检测萝卜硫素对细胞上清中乳酸脱氢酶(LDH)、丙二醛(MDA)、超氧化物歧化酶(SOD)含量的影响,免疫印迹检测萝卜硫素对细胞中JAK2/STAT3信号通路相关蛋白表达水平的影响.结果 与正常对照组相比,IRI组细胞相对存活率显著降低(P＜0.05), LDH及MDA含量显著升高(P＜0.05),而SOD活力则显著降低(P＜0.05),并且JAK2和STAT3磷酸化水平显著升高(P＜0.05);相对于IRI组而言,细胞经过不同浓度萝卜硫素及SAR302503处理后,细胞相对存活率显著升高(P＜0.05), LDH及MDA含量显著降低(P＜0.05), SOD活力则显著升高(P＜0.05),并且JAK2和STAT3磷酸化水平显著降低(P＜0.05).结论 萝卜硫素对缺血再灌注诱导的心肌细胞损伤具有保护作用,其作用机制可能与抑制JAK2/STAT3信号通路活化有关.“,”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-l) of sulforaphane and JAK2 inhibitor (SAR302503), before exposure to hypoxia (95％N2-5％C02) 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.