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目的探讨偶联葡萄糖的纳米金颗粒(Glu-GNPs)对人A549细胞的放射增敏作用及其机制。方法噻唑蓝(MTT)法检测低浓度(≤20 nmol/L)Glu-GNPs联合放射对A549细胞存活的影响,克隆形成检测Glu-GNPs对A549细胞的放射增敏作用,流式细胞仪(FCM)检测细胞周期及其凋亡。结果低浓度Glu-GNPs对A549细胞生长无明显抑制,联合X射线后具有抑制作用,在15 nmol/L范围内,随浓度增大,抑制作用增强;15 nmol/LGlu-GNPs对A549细胞有放射增敏作用,由Dq、Do计算放射增敏比(SER)分别为1.93、1.10;Glu-GNPs、单纯放射均可诱导细胞凋亡,凋亡率分别为(7.64±1.43)%、(13.46±1.99)%,联合放射组凋亡率为(21.43±1.04)%,显著高于前两组(P<0.01);Glu-GNPs作用后,细胞周期发生变化,表现为S期减少,G2/M期增加(P<0.05)。结论 Glu-GNPs对人肺腺癌细胞株A549具有放射增敏作用,其机制可能为抑制细胞亚致死损伤修复,阻滞细胞于G2/M期,并诱导细胞凋亡。
Objective To investigate the radiosensitization effect of glucose-conjugated gold nanoparticles (GNPs) on human lung adenocarcinoma A549 cells and its mechanism. Methods MTT assay was used to detect the effect of low concentration (≤20 nmol / L) Glu-GNPs combined with radiation on A549 cell viability. Clonogenic assay was used to detect the radiosensitization effect of Glu-GNPs on A549 cells. Flow cytometry ) To detect cell cycle and apoptosis. Results Low concentrations of Glu-GNPs showed no significant inhibition on the growth of A549 cells, but inhibited the growth of A549 cells. The combination of X-ray and low concentration of Glu-GNPs inhibited the proliferation of A549 cells with increasing concentration of 15 nmol / L. (SER) were 1.93 and 1.10, respectively. Glu-GNPs and radiotherapy alone could induce apoptosis, the apoptotic rates were (7.64 ± 1.43)% and (13.46 ± 1.99%). The apoptosis rate in the combined radiotherapy group was (21.43 ± 1.04)%, which was significantly higher than that in the first two groups (P <0.01). After Glu-GNPs treatment, the cell cycle changed, Period increased (P <0.05). Conclusion Glu-GNPs have a radiosensitizing effect on human lung adenocarcinoma cell line A549. The possible mechanism is that Glu-GNPs can inhibit the repair of sublethal injury, arrest cells in G2 / M phase and induce apoptosis.