BMSC-CM通过抑制Notch1信号通路减轻H2O2诱导的神经干细胞凋亡

目的 探讨骨髓间充质干细胞条件培养基( BMSC-CM)对氧化应激损伤的神经干细胞( NSCs)的保护作用,以及Notch1信号通路在其中所发挥的作用.方法 通过使用过氧化氢(H2O2)来模拟氧化应激环境,采用流式细胞仪检测NSCs的凋亡率. Western blot法检测Notch1蛋白、Hes1蛋白、含半胱氨酸的天冬氨酸水解酶 3 蛋白 ( Caspase-3 )、Caspase-9、Bcl-2相关蛋白(Bax)蛋白和B细胞淋巴瘤蛋白2 (Bcl-2)的表达量.结果 结果表明,BMSC-CM 可以降低H2O2引起的氧化应激环境的损害. BMSC-CM 可以抑制Notch1信号通路,提高神经干细胞的存活率.结论 BMSC-CM可以通过抑制Notch1 信号通路来中和氧化应激损伤对NSCs细胞凋亡的影响.

BMSC-CM reduces the effects of oxidative stress damage on neural stem cells by inhibiting Notch1 signaling pathway

Objective To investigate the protective effect of bone marrow mesenchymal stem cell conditioned medi-um (BMSC-CM) on oxidative stress-injured neural stem cells (NSCs) and the role of Notch1 signaling pathway Methods The oxidative stress environment was simulated by hydrogen peroxide ( H2O2) , and the apoptosis rate of NSCs was detected by flow cytometry. Western blot was used to detect the expression of Notch1, Hes1, Caspase-3, Caspase-9, Bax and Bcl-2. Results BMSC-CM could significantly attenuate oxidative stress environment. BMSC-CM could inhibit Notch1 signaling pathway and improve the survival rate of neural stem cells. Conclusion These results indicate that BMSC-CM could neutralize the effect of oxidative stress injury on NSCs by inhibiting Notch1 signaling pathway.