芍药内酯苷对MPP^+所致PC12细胞损伤的保护机制  

Involvement of Mitochondria-Mediated Pathway and Akt/GSK3β Signaling in Protective Action of Albiflorin Against MPP^+-Induced PC12 Cells Apoptosis

作　　者：胡馨予[1] 王雪[2] 卢文倩[2] 胡爽[2] 张欣蕊[2] 刘洋[3] 

机构地区：[1]长春医学高等专科学校临床医学部,长春130012 [2]吉林大学生命科学学院,长春130012 [3]吉林农业大学食药用菌教育部工程研究中心,长春130118

出　　处：《中国药学杂志》2016年第17期1467-1471,共5页Chinese Pharmaceutical Journal

基　　金：国家自然科学基金资助项目(81402955);吉林省教育厅"十二五"科学技术研究项目(2014B033)

摘　　要：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 determine the neuro-protective effects of albiflorin against MPP^＋ -induced PC12 cells death and related molecular mechanisms. METHODS PC12 cells were treated with 4 mmol·L^-1 MPP^＋ to establish apoptotic cell models. MTT^＋ method, DCFH-DA staining, JC-1 staining and Western Blot were used to determine the changes of cell viability, intracellular ROS concentration, mitochondrial membrane potential and the expression of Bcl-2 and Bcl-Xl, and the phosphoration of Akt/GSK3β in PC12 cells. RESULTS Albiflorin showed significantly nenro-protective effects against MPP＋ -induced cell damage. Results showed that albiflorin enhanced the cell viability, reduced intracellular ROS level and caspase 3 activation, restored the mitochondrial membrane potential, increased the expression of Bcl-2 and Bcl-X1, and enhanced the phosphoration of Akt/GSK3β. CONCLUSION Albiflorin shows neuro-protective effects against MPP^＋ -induced PC12 ceils damage via mitochondrial-dependent pathway and Akt/GSK3β signaling.

关 键 词：芍药内酯苷 1-甲基-4-苯基吡啶离子 嗜铬瘤细胞 神经保护 

分 类 号：R965[医药卫生—药理学]