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  

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

作　　者：周海红[1] 刘运林[2] 肖颂华[3] 刘军[3] 吕瑞妍[3] 赵斌[1] 

机构地区：[1]广东医学院附属医院神经内科,湛江524001 [2]山东省泰安市中心医院神经内科,271000 [3]中山大学附属第二医院神经内科,广州510120

出　　处：《中华神经医学杂志》2009年第5期464-467,共4页Chinese Journal of Neuromedicine

基　　金：国家自然科学基金（30870750）;广东省医学科研基金（B2008044）

摘　　要：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mSOs）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C17．2NSCs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。Objective To observe the effects of exogenous basic fibroblast growth factor （bFGF） on radiationqnduced apoptosis ofC17.2 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 rain 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±0.31）% 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）. Conclusion Exogenous bFGF offers protection of C17.2 NSCs against radiation-induced apoptosis, and extraeellular signal-regulated kinasesl/2 （ERK1/2） plays a role in this protective effect.

关 键 词：碱性成纤维细胞生长因子 细胞外信号调节激酶1/2 细胞凋亡 神经干细胞 

分 类 号：R686[医药卫生—骨科学]