中文摘要：

目的 探讨莱菔硫烷（sulforaphane,SFN）预处理对高糖诱导心肌细胞线粒体损伤的保护作用.方法 用高糖（33 mmol/L）作用于H9c2（2-1）大鼠心肌细胞24 h建立细胞高糖损伤模型,用噻唑蓝染色法检测不同剂量（1、5、7.5、10 μmol/L）莱菔硫烷预处理24 h和5μmol/L莱菔硫烷预处理不同时间（12、24、36、48 h）的细胞线粒体琥珀酸脱氢酶（succinie dehydrogenase,SDH）活性；荧光酶标仪检测细胞的活性氧（reactive oxygen species,ROS）产生速度和线粒体膜电位（mitochondrial membrane potential, MMP）；应用透射电镜观察线粒体形态.结果 与对照组比较,模型组SDH活性下降（P＜0.05）,莱菔硫烷组SDH活性显著高于模型组（P＜0.05）.与模型组比较,莱菔硫烷组（5μmol/L,24 h）ROS产生速度下降（P＜0.01）,MMP上升（P＜0.01）,线粒体损伤性形态变化及细胞早期凋亡形态改变减轻.结论 莱菔硫烷能够抑制高糖对心肌细胞线粒体造成的损伤.

英文摘要：

Objective To investigate the influence of sulforaphane （SFN） on the H9c2 （2-1） myocardial cell exposed to a high level of glucose.Methods H9c2（2-1） cells were cultured in vitro,the myocardial mitochondrial injured model was made by high level of glucose （33 mmol/L）.The model was pretreated by different doses of SFN （1,5,7.5,10 μmol/L） for 24 h and was pretreated by 5 μmol/L SFN for different periods （12,24,36,48 h）,then succinic dehydrogenase（SDH） activity were detected by thiazolyl blue staining.Reactive oxygen species （ROS） and mitochondrial membrane potential （MMP） were detected by fluorescent ELISA.Mitochondrial morphorlogy was observed by transmission electron microscope.Results Compared to control group,the SDH activity of model group decreased （P ＜ 0.05）.And the SDH activity of SFN groups was higher than that of model group （P ＜ 0.05）.Compared to model group,ROS production decreased （P ＜0.01） and MMP increased（P ＜0.01） by SFN （5 μmol/L,24 h） pretreatment.SFN pretreatment alleviated the symptoms that mitochondrial injuries and celluar apoptosis caused by high glucose.Conclusion SFN prevents high glucose-induced mitochondrial impairment of myocardial cell in vitro.