过氧化氢诱导PC12细胞凋亡及芍药苷的保护作用

 目的探讨过氧化氢诱导PC12细胞凋亡及芍药苷保护作用的可能机制。方法MTT测定细胞存活率,流式细胞仪测定细胞凋亡率,DCFH-DA为细胞内荧光探针,测定细胞内ROS浓度,流式细胞仪检测线粒体跨膜电位。结果200μmol·L^-1H₂O₂可诱导PC12细胞凋亡,细胞内ROS浓度增加,细胞线粒体跨膜电位明显下降。预先经过0.1,1和10μmol·L^-1浓度的芍药苷处理后,H₂O₂诱导的PC12细胞凋亡明显减少,同时明显减弱H₂O₂对细胞内ROS浓度和线粒体跨膜电位的影响。结论芍药苷可抑制过氧化氢诱导PC12细胞凋亡,其作用机制可能与其抑制细胞内ROS累积,稳定细胞线粒体跨膜电位有关。

Hydrogen Peroxide- Induced PC12 Cells Apoptosis and the Protective Effect of Paeoniflorin

OBJECTIVE To explore the possible mechanism of hydrogen peroxide-induced PC12 cells apoptosis and the protective effect of paeoniflorin.METHODS MTT assay for cell survival,flow cytometric detection of apoptotic cells,DCF assay for reactive oxygen species(ROS) and flow cytomet ric assay was performed to determine the mitochondral membrance potential in PC12 cells.RESULTS 200 μmol·L^-1H₂O₂ induced PC12 cells apoptosis,paeoniflorin decreased H₂O₂-induced intracellular accumulation of ROS and increased mitochondral membrance potential.CONCLUSION Paeoniflorin inhibited H₂O₂-induced apoptosis in PC12 cells.The mechanism is related to reducing H₂O₂induced intracellular accumulation of ROS and preventing loss of MMP in PC12 cells.