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目的:研究碱性成纤维细胞生长因子(bFGF)抑制放射性诱导小鼠C17.2神经干细胞凋亡的作用。方法:用直线加速器进行总剂量为8 Gy外照射C17.2神经干细胞建立放射损伤细胞模型,将处理后的C17.2神经干细胞悬液以1×108/L的浓度接种于96孔板中,每孔加细胞悬液200μl,然后分别加入bFGF 0(对照),25,50和100μg/L干预24 h处理。用4-甲基偶氮唑盐法检测细胞活性并拟合生存曲线,用流式细胞仪检测细胞凋亡率。结果:随bFGF浓度增加,放射诱导后的C17.2神经干细胞增殖比明显增加(P<0.01),呈现明显剂量-效应关系(r=0.628,P<0.01)。在一定放射剂量下,随着bFGF浓度增加C17.2神经干细胞生存曲线右移,表明bFGF能够提高神经干细胞的放射耐受性(r=0.569,P<0.01)。bFGF为100μg/L时,C17.2神经干细胞活性最强,且无细胞毒性作用。流式细胞仪测定的对照组C17.2神经干细胞凋亡率明显高于bFGF 25和50μg/L(P<0.01)处理组,并且凋亡率在bFGF 25,50和100μg/L组间也存在显著差异(P<0.01)。结论:bFGF能显著抑制放射诱导的小鼠C17.2神经干细胞凋亡,其机制有待进一步研究。
AIM: To investigate the effect of basic fibroblast growth factor (bFGF) on the apoptosis of C17.2 neural stem cells induced by radiation in mice. Methods: Radiation injury model of C17.2 neural stem cells was established by using a linear accelerator with a total dose of 8 Gy. The irradiated C17.2 neural stem cell suspension was seeded into 96-well plates at the concentration of 1 × 108 / L, Each well was added with 200 μl of cell suspension, then bFGF 0 (control) was added and treated with 25, 50 and 100 μg / L for 24 h. The cell viability was measured by 4-methylazolium salt method and the survival curve was fitted. The apoptosis rate was detected by flow cytometry. Results: With the increase of bFGF concentration, the proliferation ratio of C17.2 neural stem cells after radiotherapy was significantly increased (P <0.01), showing a significant dose-effect relationship (r = 0.628, P <0.01). At a certain dose of radiation, bFGF increased the survival of neural stem cells (r = 0.569, P <0.01) as the bFGF concentration increased to the right of the survival curve of C17.2 neural stem cells. When bFGF was 100μg / L, C17.2 neural stem cells had the strongest activity with no cytotoxic effect. The apoptosis rate of C17.2 neural stem cells in control group was significantly higher than that in bFGF 25 and 50μg / L groups (P <0.01) by flow cytometry, and the apoptosis rates were also found in bFGF 25, 50 and 100μg / L groups Significant difference (P <0.01). CONCLUSION: bFGF can significantly inhibit the apoptosis of C17.2 induced by radiation in mice, and its mechanism remains to be further studied.