外源性bFGF抑制辐射诱导的C17.2神经干细胞凋亡的实验研究

目的 观察外源性碱性成纤维细胞生长因子(bFGF)对辐射诱导的C17.2神经干细胞(NSCs)凋亡的影响,探讨细胞外信号调节激酶1/2(ERK1/2)在bFGF对辐射诱导的C17.2 NSCs凋亡的抑制效应中的作用. 方法 以直线加速器照射C17.2NSCs建立离体放射性损伤模型.MTT法检测细胞活性,流式细胞仪检测不同浓度的外源性bFGF和U0126对细胞凋亡的影响. 结果 外源性bFGF浓度为0～100ng/mL时,细胞凋亡率可由(12.78±1.04)%降低至(4.83±0.31)%,组间比较差异有统计学意义(P<0.05);加入U0126后细胞凋亡率为(8.42±0.71)%.DMSO对照组为(4.71±0.42)%,差异有统计学意义(P<0.05). 结论 外源性bFGF对辐射引起的C17.2 NSCs凋亡具有抑制作用,ERK1/2参与该效应.

Extracellular signal-regulated kinases1/2 is involved in the inhibition of radiation-induced apoptosis of C17.2 neural stem cells by exogenous basic fibroblast growth factor

Objective To observe the effects of exogenous basic fibroblast growth factor (bFGF) on radiation-induced apoptosis of C 17.2 neural stem cells (NSCs) and explore the role of ERK1/2 in this process. Methods C17.2 NSCs were subjected to irradiation exposure generated by a linear accelerator followed by treatment with different concentrations of bFGF 5 min after the exposure. The cell viability after the treatments was assessed using MTT assay, and the effects of exogenous bFGF and U0126 on radiation-induced apoptosis of the cells were analyzed with flow cytometry. Results The apoptotic rate of the irradiated cells decreased from (12.78±1.04)% to (4.83±0.3 I)% as the concentration ofbFGF increased from 0 to 100 ng/mL. The apoptotic rates of the cells after treatment with U0126 and DMSO were (8.42±0.71)% and (4.71±0.42)%, respectively, showing a significant difference (P<0.05). Conehlsion Exogenous bFGF offers protection of C17.2 NSCs against radiation-induced apoptosis, and extracellular signal-regulated kinases 1/2 (ERK1/2) plays a role in this protective effect.