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目的:本研究旨在评估依托泊苷(etoposide,VP-16)、顺铂(cisplatin,DDP)(EP方案)联合重组人血管内皮抑制素对小细胞肺癌(small-cell lung cancer,SCLC)NCI-H446细胞的促凋亡和抑制细胞增殖的协同作用。方法:EP方案、重组人血管内皮抑制素单药以及EP方案联合重组人血管内皮抑制素作用于NCI-H446细胞72h后,采用CCK-8(cell counting kit-8)法测定药物对NCI-H446细胞的增殖抑制作用,FCM检测药物对NCI-H446细胞的细胞周期分布的影响,ELISA法检测药物对NCI-H446细胞分泌血管内皮细胞生长因子(vascular endothelial cell growth factor,VEGF)水平的影响。结果:EP方案联合重组人血管内皮抑制素的细胞增殖抑制率明显高于EP方案组(P<0.01)。EP方案组和EP方案联合重组人血管内皮抑制素组的NCI-H446细胞大多被阻滞于G1期,EP方案联合重组人血管内皮抑制素组的NCI-H446细胞凋亡率显著高于EP方案组(P<0.01)。与EP方案和重组人血管内皮抑制素单药相比,EP方案联合重组人血管内皮抑制素可显著抑制NCI-H446细胞分泌VEGF(P<0.05)。结论:EP方案联合重组人血管内皮抑制素在抑制SCLCNCI-H446细胞增殖和促细胞凋亡方面,具有协同作用。
Objectives: This study was designed to evaluate the effects of etoposide (VP-16), cisplatin (DDP) (EP regimen) combined with recombinant human endostatin on small cell lung cancer (SCLC) NCI -H446 cells and the synergistic effect of inhibiting cell proliferation. Methods: After 72 h treatment of NCI-H446 cells with EP regimen, recombinant human endostatin monotherapy and EP regimen combined with recombinant human endostatin, the effect of drugs on NCI-H446 cells was evaluated by CCK-8 (cell counting kit-8) The effect of drugs on the cell cycle distribution of NCI-H446 cells was detected by FCM. The effect of drugs on the secretion of vascular endothelial cell growth factor (VEGF) in NCI-H446 cells was detected by ELISA. Results: The cell proliferation inhibition rate of EP regimen combined with recombinant human endostatin was significantly higher than that of EP regimen (P <0.01). EPI group and EP regimen combined with recombinant human endostatin group NCI-H446 cells were mostly blocked in the G1 phase, EP regimen combined with recombinant human endostatin group NCI-H446 cell apoptosis rate was significantly higher than the EP program Group (P <0.01). Compared with EP regimen and recombinant human endostatin monotherapy, EP regimen combined with recombinant human endostatin significantly inhibited VEGF secretion in NCI-H446 cells (P <0.05). Conclusion: EP regimen with recombinant human endostatin has a synergistic effect in inhibiting the proliferation and promoting apoptosis of SCLCNCI-H446 cells.