摘要
目的探讨PI3K/Akt信号在β样淀粉蛋白(Aβ1-40)引起的PC12细胞凋亡中的作用及依达拉奉(MCI-186)对其影响。方法采用流式细胞学检测细胞凋亡,Western blot法检测磷酸化Akt及总Akt水平,观察MCI-186对其保护作用。结果模型组中各时间点Akt Ser473的磷酸化水平与对照组比较均降低而保护组各时间点Akt Ser473的磷酸化水平均有明显的升高(P<0.05),保护组中细胞凋亡率较模型组显著降低(P<0.01)。结论Aβ1-40主要通过抑制磷酸化Akt水平,进而诱导PC12细胞凋亡。MC-186通过激活PI3K/Akt信号传导途径,发挥拮抗细胞凋亡的作用,最终达到保护神经细胞的目的。
Objective To investigate the effects of edaravone （MCI-186）on apoptosis of PC12 cells induced by β- amyloid （Aβ） and its possible relationship with PI3 K/Akt. Methods The flow cytometry analysis was used to detect apoptosis, and Western blot was used to detect Akt phosphorylation level and total Akt for observing the protective effect of MCI- 186 on Aβ induced apoptosis in PC12 ceils. Results Akt Ser473 decreased in group of model at different time points compared to normal control group （P 〈 0.05 ）, Akt Ser473 increased and apoptosis rate was decreased significantly in protection group（P 〈0.01 ）. Conclusion Aβ1-40 induced PCI2 cells apoptosis through inhibiting Akt phosphorylation level;on the contrast,MCI-186 protectes against Aβ-induced cytotoxicity and decrease apoptosis cells under Aβ1-40 treatment by PI-3K/ Akt signal transduction pathway.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2010年第1期12-15,共4页
Journal of Apoplexy and Nervous Diseases
基金
黑龙江省教育厅资助课题(1154205)
