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目的考察芍药内酯苷对1-甲基-4-苯基吡啶离子(MPP+)诱导的PC12细胞损伤的保护作用及分子机制。方法 4mmol·L-1MPP+处理大鼠嗜铬细胞瘤细胞株(pheochromocytoma cells,PC12),构建细胞凋亡模型。采用药物预处理给药方法,四甲基偶氮唑蓝(MTT)法测定细胞存活率,DCFH-DA荧光染色法测定胞内活性氧簇(ROS)浓度,JC-1荧光探针染色法测定线粒体跨膜电位变化,Western Blot测定Bcl-2、Bcl-Xl、Cleaved Caspase 3蛋白表达以及Akt/GSK3β磷酸化情况。结果芍药内酯苷可明显提高MPP+诱导的PC12细胞的细胞存活率,抑制胞内ROS水平以及caspase 3的激活;减弱MPP+引起的线粒体跨膜电位的减弱,增加Bcl-2和Bcl-Xl蛋白的表达量,提高Akt/GSK3β磷酸化水平。结论芍药内酯苷可通过线粒体依赖途径及Akt/GSK3β通路有效抑制MPP+诱导的PC12细胞凋亡。
Objective To investigate the protective effect of paeoniflorin on the injury of PC12 cells induced by 1-methyl-4-phenylpyridinium ion (MPP +) and its molecular mechanism. Methods The rat pheochromocytoma cells (PC12) were treated with 4 mmol·L-1 MPP + to establish a cell apoptosis model. The cell viability was determined by MTT assay, intracellular reactive oxygen species (ROS) concentration was determined by DCFH-DA staining, and fluorescence staining was used to determine the concentration of intracellular reactive oxygen species (ROS) Mitochondrial transmembrane potential changes, Western Blot determination of Bcl-2, Bcl-Xl, Cleaved Caspase 3 protein expression and Akt / GSK3β phosphorylation. Results Paeoniflorin significantly increased cell viability induced by MPP +, inhibited intracellular ROS and activation of caspase 3, decreased the mitochondrial transmembrane potential induced by MPP +, increased the expression of Bcl-2 and Bcl-Xl The level of Akt / GSK3βphosphorylation was increased. Conclusion Paeoniflorin can effectively inhibit the apoptosis of PC12 cells induced by MPP + through the mitochondria-dependent pathway and Akt / GSK3β pathway.