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目的:通过观察肿瘤血管生成抑制剂内皮抑素和放疗联合应用后对肺腺癌A549细胞凋亡率及HIF-1、VEGF表达的影响,初步探索血管内皮抑素的放疗增敏机制。方法:Hoechst染色法观察不同方法对细胞凋亡率的影响,ELISA法检测不同时间点HIF-1、VEGF的表达情况。结果:联合治疗后的细胞凋亡率高于其它各组(P<0.05),同时给予内皮抑素及放疗对HIF-1的抑制效果最好;联合治疗对VEGF的抑制效果最显著(P<0.05),但是并无给药时序的差别。结论:内皮抑素联合放疗能协同促进肺腺癌A549细胞凋亡,其协同作用机制可能是通过抑制放疗诱导的HIF-1、VEGF的表达,达到放疗增敏作用。
OBJECTIVE: To investigate the effects of endostatin combined with radiotherapy on the apoptosis of lung adenocarcinoma A549 cells and the expression of HIF-1 and VEGF, and to explore the radiosensitization mechanism of endostatin. Methods: Hoechst staining was used to observe the effects of different methods on apoptosis rate. ELISA was used to detect the expression of HIF-1 and VEGF at different time points. Results: The apoptosis rate of the combined treatment group was higher than that of other groups (P <0.05), and at the same time endostatin and radiotherapy had the best HIF-1 inhibitory effect. The combination therapy had the most significant inhibitory effect on VEGF (P < 0.05), but there was no difference in timing of administration. Conclusion: Endostatin combined with radiotherapy can synergistically promote the apoptosis of lung adenocarcinoma A549 cells. The synergistic mechanism may be that radiotherapy-induced sensitization may be achieved by inhibiting the expression of HIF-1 and VEGF induced by radiotherapy.