Objective To discuss the toxicity mechanism of recombinantβ-amyloid peptide 1~42( Aβ1~42 ) on U251 cell.Methods U251 glioma cells were divided into normal control and experimental groups cultured in vitro.The experimental group was divided into 0.5, 1,5,10,20 μmol/L subgroups.MTT assay was used to detect cell survival,AO/EB fluorescent assay technique,electron microscopy and Western blot were used to test the expressions of bax,bcl-2.Results The growth inhibition rate was increased obviously through U251 cells growth curve.The apoptosis characteristic of U251 treated by Aβ1~42 was found by fluorescence and electron microscopy,and the expression of Bcl-2 was decreased and the expression of Bax was increased.Conclusions U251 cell damage caused by Aβ1~42 is mainly through the way of apoptosis.%目的：探讨重组人β淀粉样蛋白（ Aβ）1～42对人神经胶质瘤细胞U251的凋亡作用。方法体外培养的神经胶质瘤细胞 U251分为对照组和实验组。实验组根据Aβ1～42作用终浓度的不同，分为0.5、1、5、10和20μmol／L 5个亚组，分别培养24 h 后，采用 MTT 法检测细胞存活， AO／EB光镜荧光染色技术、透射电镜以及Western印迹技术检测凋亡蛋白Bax、Bcl-2研究Aβ1～42损伤U251的途径。结果 Aβ1～42作用神经胶质瘤细胞24 h后，Aβ1～42剂量依赖性地引起U251细胞的代谢率减少；荧光染色及电镜观察经Aβ1～42处理的 U251细胞表现出凋亡细胞的特征；Western印迹检测发现Bcl-2表达量随剂量的增加而明显下调，而Bax的表达则相反。结论 Aβ1～42对U251细胞的损伤可能主要通过细胞凋亡的途径。
展开▼
