摘要
目的探讨β-淀粉样蛋白(Aβ1-40)诱导PC12细胞凋亡,对突触素的表达影响。方法星形胶质细胞诱导PC12细胞分化为神经元样细胞。PC12细胞随机分为7组:Aβ1-40(0h)组～Aβ1-40(24h)组和对照组。应用MTT法检测细胞生存率,吖啶橙染色、流式细胞仪观察PC12细胞凋亡情况,应用免疫荧光技术检测突触素的表达变化。结果 Aβ1-40作用PC12细胞6h时,细胞生存率明显下降,细胞出现凋亡特征改变,细胞凋亡率最高,与对照组、其他各时间点比较,差异有统计学意义(P<0.05);Aβ1-40作用PC12细胞4h时,突触素明显减少,与对照组、其他各时间点相比,差异有统计学意义(P<0.05)。结论在Aβ1-40诱导大量PC12细胞明显出现凋亡特征之前,Aβ已经引起PC12细胞突触素明显减低,β-淀粉样蛋白(Aβ)可能引起PC12细胞早期神经突触损伤。
Objective To investigate the effects of beta-amyloid（Aβ1-40） treatment on synaptophsin expression in PC12 cells.Methods Astrocytes were used to induce the PC12 cells into neurons-like cells.Then PC12 cells were grouped into 7 groups randomly：Aβ1-40（0h）group～ Aβ1-40（24h）group and control group.We measured the rate of cell viability by MTT methods,investigated the apoptosis of the PC12 cells by acridine orange staining and flow cytometer,and measured the expression changes of synaptophsin by immunofluorescence technique.Results At 6h after Aβ1-40treatment,the rate of PC12 cell viability decreased obviously,the apoptosis features of the cells appeared,and the rate of the apoptosis was the highest.This group showed significant difference compared with the control group and other groups.At 4h after Aβ1-40treatment,synaptophsin decreased obviously,and this group showed significant difference compared with the control group and other groups.Conclusion Before the apoptosis features appeares obviously,Aβ1-40has already caused obvious reduction of synaptophsin in PC12 cells,which suggests that beta-amyloid may cause early damage in PC12 cells.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2010年第9期815-818,共4页
Journal of Apoplexy and Nervous Diseases
基金
辽宁省博士科研启动基金(No.20091106)
