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中文摘要：
目的建立阿尔茨海默病（AD）的细胞模型,并探讨β淀粉样蛋白25-35（Aβ25-35）对细胞骨架的神经毒性机制。方法采用MTT法检测不同浓度的Aβ25-35对PC12细胞存活率的影响,应用4’6-二脒基-2-苯基吲哚（DAPI）染色法和TUNEL法检测细胞凋亡,免疫细胞化学法和鬼笔环肽（phalloidin）染色观察细胞骨架的形态变化。结果 Aβ25-35经过＂老化＂处理后,可以明显引发PC12细胞死亡,导致PC12细胞发生凋亡,并具有剂量依赖性（P〈0.05）。Aβ25-35也可以引起细胞骨架解体,同样具有剂量依赖性（P〈0.05）。结论 PC12细胞的细胞骨架对Aβ25-35的神经毒性非常敏感,细胞骨架的解体很可能是AD重要的病理学改变,同时Aβ是AD发病机制的关键分子。
英文摘要：
Objective To establish the cell model of Alzheimer＇s disease（ AD） and investigate the amyloid betapeptides25-35（ Aβ25-35） neurotoxicity to cytoskeleton. Methods PC12 cells were cultured and treated with Aβ25-35,and cell survival was analyzed by MTT assay. Cell apoptosis was visualized with DAPI staining and TUNEL method.Immunocytochemistry and phalloidin staining were used to label cytoskeletons in PC12 cells. Results Aβ25-35 obviously induced the PC12 cells death and lead to PC12 cells apoptosis with dose dependency（ P〈0. 05）. Aβ25-35 gave rise to the disintegration of cytoskeletons with dose dependency（ P〈0. 05）. Conclusion PC12 cell cytoskeletons are sensitive to Aβ25-35 neurotoxicity. The disintegration of cytoskeleton probably is the important pathological alteration in AD,and Aβ is a key molecule for AD pathogenesis.
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