摘要
目的β-淀粉样蛋白（Aβ）是老年斑（SP）和血管壁淀粉样沉积的主要成份．它在早老性痴呆（AD）病理生理过程中的作用机制还不清楚。方法：本实验通过神经细胞培养，采用MTT比色法和免疫组化法，结合图像分析技术研究Aβ25—35对大鼠大脑皮质神经元和海马神经元存活和生长的作用，为揭示Aβ在AD发病中的作用提供资料。结果：（1）MTT法测得的“老化”Aβ25－35（20μmol／L）组的OD值比5μmol／L组，10μmol／L组及未老化的Aβ25－35（20μmol／L）组的OD伍均明显降低（P＜0.05），其它各组之间无明显差异。（2）形态学测量“老化”的Aβ25－35（20μamol／L）组．10μmol／L组的神经元胞体的最长径，最短径及平均突起长度也显著低于其它各组（P＜0.05）。结论：Aβ25－35片段对神经元具有神经毒作用．而这种作用又与Aβ的浓度和聚集状态有密切关系。
Objective: β- amyloid protein (Aβ)is a primary constituent in senile plaque (SP)in Alzheimer's disease (AD). The exact role of this peptide in the celluar mechanism underlying the disease process is not clearly defined. The goal of this study is to extend understanding of neurotoxic effect of Aβ25- 35 on the neurons. Methods: Using MTT assay and immunocyto chemistry combined with morphometry in cell culture. Results: (1 )The results of MTT assay show that average OD valtles of aging Aβ25 - 35 (20μmol/L)are lower than that of control group Aβ25 - 35 (5μmol/L ),group 100μmol/L and group Aβ25 - 35 (20μmol/L)(P＜0. 05 ) in hippocampal and cerebral cortex neurons. (2)The morphologic changes show that the average maximum and minimum diameters of neurons in aging Aβ25 - 35 (20μmol/L) group are decreased significantly as compared with those of other groups (P＜0.05 ). Conclusion: The results suggest that Aβ25 - 35 process the neurotoxicity.. which associates closely with the concentration and aggregation of this peptide.
出处
《农垦医学》
1999年第4期240-243,共4页
Journal of Nongken Medicine
