IGF-1对MPP^+诱导PC12细胞凋亡的保护作用及其机制  

Protective mechanism of IGF-1 on MPP^+ induced neurotoxicity in PC12 cells

作　　者：黄露麒[1] 孙欣[1] 吴艳[1] 孙圣刚[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院,湖北武汉430022

出　　处：《中风与神经疾病杂志》2010年第3期218-221,共4页Journal of Apoplexy and Nervous Diseases

摘　　要：目的探讨胰岛素样生长因子-1(IGF-1)对1-甲基-4-苯基吡啶离子(MPP+)诱导的PC12细胞凋亡的保护作用及机制。方法以250μmol/L的MPP+损伤PC12细胞作为帕金森病(PD)细胞模型,实验分组如下:空白对照组、MPP+组,IGF-1+MPP+组和抑制剂组。抑制剂组再分为:(1)空白对照组;(2)MPP+组;(3)IGF-1组;(4)IGF-1+MPP+组;(5)MPP++LiCL组;(6)IGF-1+MPP++LiCL组。孵育24h后采用AO-EB法检测细胞凋亡率;采用MTT法检测细胞存活率;孵育4h之后采用Western Blot免疫印迹法检测糖原合成酶激酶-3β(GSK-3β)、phospho-GSK-3β蛋白表达。结果(1)100nmol的IGF-1对MPP+处理的PC12细胞有保护作用,减少了MPP+所致的细胞凋亡。(2)LiCL起到了与IGF-1相似的对PC12细胞的保护作用。(3)总GSK-3β含量各处理组没有太大改变,但磷酸化的GSK-3β含量IGF-1组高于与MPP+单独处理组。结论IGF-1可减少MPP+所致的细胞凋亡,其保护作用与上调磷酸化的GSK-3β的表达相关。Objective To investigate the protective mechanism of IGF-1 on MPP＋ induced neurotoxicity in PC12 cells. Methods PC12 cells impaired by MPP＋（250μmol/L）were used as the cell model of Parkinson＇s disease. The cultured cells were divided into such groups：control group,MPP＋ group,MPP＋＋IGF-1 group and inhibitor group. Inhibitor group was divided into control subgroup,MPP＋ subgroup,IGF-1 subgroup,IGF-1＋MPP＋ subgroup,IGF-1＋MPP＋＋LiCL subgroup and MPP＋＋LiCL subgroup. After incubation for 24h,methyl thiazolyl tetrazolium（MTT）was used to assay the viability of the PC12 cells. After incubation for 4h,western blot was used to detect the expression level of GSK-3β,phospho-GSK-3β. Results 100nmol/L IGF-1 protected PC12 cells from MPP＋. LiCL took a protective effect on PC12 cells as well as IGF-1.The level of total-GSK-3βhad not changed after all the treatment,however,the level of phospho-GSK-3β is higher in IGF-1 treated group than which treated with MPP＋. Conclusion These findings indicate that IGF-1 protects against apoptosis in PC12 cells exposed to MPP＋,that protective effect is associated with an up-regulation of phospho-GSK-3β.

关 键 词：IGF-1 MPP+ PC12细胞 凋亡 GSK-3Β 

分 类 号：R742.5[医药卫生—神经病学与精神病学]