BMSC-CM通过抑制Notch1信号通路减轻H_2O_2诱导的神经干细胞凋亡

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

目的探讨骨髓间充质干细胞条件培养基(BMSCCM)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(H_2O_2)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H_2O_2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 BMSCCM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。

Objective To investigate the protective effect of bone marrow mesenchymal stem cell conditioned medium（ 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（ H2 O2）,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. BMSCCM 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.