IGF-1通过PI3K/Akt通路抑制MPP^+诱导PC12细胞凋亡机制的研究  

IGF-1 inhibited the MPP^+ induced apoptosis of PC12 cells via PI3K /Akt signaling pathway

作　　者：黄露麒 王万铭 

机构地区：[1]武汉市长江航运总医院神经内科,湖北武汉430000

出　　处：《中风与神经疾病杂志》2014年第10期897-899,共3页Journal of Apoplexy and Nervous Diseases

摘　　要：目的探讨胰岛素样生长因子-1(insulin-like growth factor-1,IGF-1)对1-甲基-4-苯基吡啶离子(1-methyl-4-phenylpyridinium,MPP+)诱导的PC12细胞凋亡的抑制作用及其潜在的作用机制。方法以250μmol/L的MPP+损伤PC12细胞作为帕金森病(Parkinson disease,PD)细胞模型。实验分组如下:空白对照组、MPP+组、IGF-1组、IGF-1+MPP+组、IGF-1+MPP++LY294002组。孵育24 h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4 h之后采用Western blot免疫印迹法检测Akt、磷酸化-Akt(phospho-Akt,p-Akt)蛋白表达。结果 (1)100 nmol的IGF-1能够显著抑制MPP+所致的细胞凋亡,对PC12细胞具有保护作用;(2)总Akt含量蛋白表达水平各处理组之间差别无统计学意义(P>0.05),但磷酸化的Akt在IGF-1+MPP+组表达高于MPP+单独处理组(P<0.05)。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Akt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^＋（ 250 μmol/L） were used as the cell model of Parkinson＇s disease. The cultured cells were divided into such groups：（ 1） control group;（ 2） MPP^＋group;（ 3） IGF-1 group;（ 4） IGF-1 ＋ MPP^＋group;（ 5） IGF-1 ＋ MPP^＋＋ LY294002 group. After incubation for 24 h,methyl thiazolyltetrazolium（ MTT） was used to assay the viability of the PC12 cells. After incubation for 4 h,Western blot was used to detect the expression level of Akt、phospho-Akt. Results（ 1） 100 nmol /L IGF-1 protect PC12 cells from MPP^＋.（ 2） The level of total-Akt had not changed after all the treatment,however,the level of phospho-Akt was higher in IGF-1 treated group than that treated with MPP^＋.Conclusion These findings indicate that IGF-1 protects against apoptosis in PC12 cells exposed to MPP^＋,the protective effect is associated with an up-regulation of phospho-Akt.

关 键 词：IGF-1 MPP^+ PC12细胞 凋亡 Akt 

分 类 号：R742.5[医药卫生—神经病学与精神病学]