bFGF基因转染对放射诱导的C17．2神经干细胞凋亡的抑制作用

Inhibitory effect of exogenous bFGF gene transfection on radiation-induced apoptosis in C17.2 neural stem cells

目的观察外源性碱性成纤维细胞生长因子（bFGF）基因转染对放射诱导的C17．2神经干细胞（NSCs）凋亡的抑制作用，为探索治疗放射性脑损伤（RE）的新途径奠定实验基础。方法以直线加速器照射C17．2NSCs建立离体放射性损伤模型，流式细胞仪检测凋亡率和坏死率，MTT法检测细胞活性并拟合生存曲线。构建含bFGF片段的真核表达体pcDNA3．1-bFGF质粒后，脂质体法转染C17．2NSCs，观察转染pcDNA3．1-bFGF质粒后细胞对放射的耐受情况，并与对照组比较。结果转染pcDNA3．1-bFGF的C17．2NSCs放射后凋亡率和死亡率均显著低于转染空质粒组和对照组（P〈0．05）。结论外源性bFGF基因转染对放射诱导的C17．2NSCs凋亡具有明显抑制作用．对RE有潜在的治疗价值。

Objective To explore the effect of gene transfection of exogenous basic fibroblast growth factor （bFGF） on radiation-induced apoptosis in C17.2 neural stem cells （NSCs）, and establish experimental basis for clinical management of radiation injuries in brain. Methods C 17.2 NSCs were radiated by linear accelerator to establish the radiation injury model in vitro. The apoptosis and necrosis rates were detected by flow cytometry, and cell vitality was detected by MTT method. Eukaryotic expression plasmid containing bFGF, pcDNA3.1-bFGF was constructed and transfected into C17.2 NSCs by liposome method to study its effect on radiation-induced apoptosis. Survival curves were drawn accordingly. Results The apoptosis and necrosis ratios of C17.2 NSCs transfected with pcDNA3.1-bFGF were significantlylower than those of the control group and of the ones transfected with pcDNA3.1 plasmid （P〈0.05）. Conclusion Exogenous bFGF transfection has an obvious inhibitory effect on radiation-induced apoptosis in C17.2 NSCs, thus it has potent value for the treatment of radiation injury in brain and provides a basis for further research.