中文摘要：

目的研究麦冬皂苷D′对大鼠心肌细胞H9c2的细胞毒性作用,初步探讨其作用机制,为寻找其临床安全使用剂量提供依据。方法麦冬皂苷D′0.1,1,5,10,20,25和50μmo·L（-1）作用于H9c2细胞24 h。MTS法检测细胞存活率及其IC_（50）;荧光显微镜观察细胞形态变化;高内涵免疫荧光筛选检测细胞核数目变化;流式细胞仪检测其活性氧生成、线粒体膜电位和细胞凋亡率。结果麦冬皂苷D′0.1,1,5,10,20,25和50μmol·L（-1）作用于H9c2细胞24 h后,细胞存活率分别为108.9%,106.3%,91.9%,61.0%,24.8%,24.7%和24.2%,IC_（50）为9.9μmol·L（-1）;荧光显微镜检测显示细胞皱缩;高内涵免疫荧光检测显示细胞核数目减少（P〈0.05）。流式细胞术检测显示,麦冬皂苷D′0.1,1,5和10μmol·L（-1）显著升高活性氧生成量（P〈0.05）,降低线粒体膜电位（P〈0.05）,升高细胞凋亡率（P〈0.05）。结论麦冬皂苷D′对H9c2心肌细胞有明显的细胞毒性作用,该作用可能与其激活细胞凋亡通路有关。

英文摘要：

OBJECTIVE To study the cardiotoxicity of ophiopogonin D（OPD） for rat H9c2 cardio- rnyocytes. METHODS H9c2 cells were exposed to OPD＇ 0.1, 1, 5, 10, 20, 25 and 50 pmol.L-1 for 24 h. Cell viability was examined by MTS assay, and the morphological changes in H9c2 cells were quanti- fied. The cell nucleus injury was examined by high content immune fluorescence screening and the morphological changes were observed under a fluorescence microscope. After treatment with OPD＇ 0.1, 1, 5 and 10μmol. L-1 for 24 h, the effect on reactive oxygen species （ROS）, mitochondrial mem- brane potential（MMP） and apoptosis was detected by flow cytometry. RESULTS The viability was sig- nificantly reduced following exposure to OPD＇ 0.1, 1, 5, 10, 20, 25 and 50μmol- L-1 （P〈0.05, P〈0.01）. The IC50 value was 9.9 μmol. L-1 and cell shrinkage and apoptosis occurred. The levels of ROS and apoptosis rate of H9c2 cells were significantly increased after exposure to OPD＇ 0.1, 1, 5 and 10 pmol. L-1 for 24 h （P〈0.05,/：）〈0.01） and MMP markedly declined （P〈0.05, P〈0.01）. CONCLUSION OPD＇ has significent cytotoxicity on H9c2 cells. It may be related to inducing apopotsis pathways.