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目的探讨丁基苯酞(dl-3-n-Butylphthalide,NBP)对鱼藤酮诱导的帕金森病细胞模型的保护作用及其机制。方法分别使用终浓度为0.1、1、10、100μM NBP和溶剂二甲基亚砜(DMSO)预处理SH-SY5Y细胞24h后,加入终浓度为200nM的鱼藤酮处理24h建立多巴胺能细胞损伤模型,观察各组细胞形态,采用四甲基偶氮唑盐(MTT)比色法检测细胞活性,流式细胞术检测细胞凋亡率(Annexin V-FITC/PI)、线粒体膜电位(JC-1)、细胞内活性氧水平(DCFH-DA)。结果200nmol/L鱼藤酮处理SH-SY5Y细胞24h能够诱导细胞活性下降和细胞凋亡,NBP预处理后SH-SY5Y细胞存活率明显升高,细胞凋亡率降低,线粒体膜电位显著升高(P<0.05),细胞内活性氧水平显著降低(P<0.05),且随NBP浓度的增加对SH-SY5Y细胞的保护作用增强。结论NBP对鱼藤酮诱导的SH-SY5Y细胞损伤具有良好的保护作用,线粒体保护可能是其作用机制之一。
Objective To investigate the protective effect of dl-3-n-Butylphthalide (NBP) on rotenone-induced Parkinson’s disease in vitro and its mechanism. Methods SH-SY5Y cells were pretreated with 0.1, 1, 10, 100 μM NBP and DMSO for 24 h, then treated with 200 nM final concentration of rotenone for 24 h to establish a dopaminergic cell injury model. Cell morphology was determined by MTT colorimetric assay. Annexin V-FITC / PI and mitochondrial membrane potential (JC-1) were detected by flow cytometry. Intracellular reactive oxygen species (DCFH-DA). Results After treatment with 200 nmol / L rotenone for 24 h, SH-SY5Y cells could induce the decrease of cell viability and apoptosis. After NBP pretreatment, the survival rate of SH-SY5Y cells was significantly increased, the apoptosis rate was decreased and the mitochondrial membrane potential was significantly increased (P < 0.05). The level of reactive oxygen species (ROS) in cells was significantly decreased (P <0.05), and the protection of SH-SY5Y cells was enhanced with the increase of NBP concentration. Conclusion NBP has a good protective effect on rotenone-induced SH-SY5Y cell injury. Mitochondrial protection may be one of its mechanisms.