论文部分内容阅读
目的探讨二十二碳六烯酸(DHA)与顺铂(DDP)联用对食管癌细胞Eca109/DDP增殖、周期和凋亡的影响。方法采用递增药物质量浓度持续作用诱导法建立耐DDP的食管癌细胞Eca109/DDP。DHA联合DDP作用于Eca109/DDP细胞,MTT法检测Eca109/DDP细胞增殖情况;流式细胞术检测细胞周期及细胞凋亡。结果递增药物质量浓度持续作用诱导6个月后,细胞可以在含1μg/ml DDP的培养液中正常生长,其对DDP的耐药指数为15.886,所得细胞命名为耐DDP的食管癌细胞Eca109/DDP。单用DHA浓度≤1.560μg/ml时,对Eca109/DDP细胞无明显抑制作用(P>0.05),但与DDP 1μg/ml合用能显著促进DDP抑制Eca109/DDP细胞的增殖(P<0.05),并促进DDP诱导Eca109/DDP细胞周期改变、细胞凋亡增加。细胞周期表现为G1期细胞明显增多(P<0.05),S期细胞、G2期细胞明显减少(P<0.05);细胞的凋亡率明显增加(P<0.05)。结论 DHA促进DDP抑制Eca109/DDP细胞增殖可能与改变Eca109/DDP细胞周期、增加细胞凋亡有关。
Objective To investigate the effects of docosahexaenoic acid (DHA) and cisplatin (DDP) on proliferation, cell cycle and apoptosis of esophageal carcinoma cell line Eca109 / DDP. Methods Eca109 / DDP esophageal cancer cells resistant to DDP were established by the continuous induction of drug concentration. DHA combined with DDP on Eca109 / DDP cells, MTT assay Eca109 / DDP cell proliferation; flow cytometry cell cycle and apoptosis. The results of incremental drug concentration continued role of 6 months after induction, the cells can be normal in the culture medium containing 1μg / ml DDP, the resistance index of DDP 15.886, the resulting cells named DDP-resistant esophageal cancer cells Eca109 / DDP. DHA alone did not significantly inhibit the proliferation of Eca109 / DDP cells (P> 0.05), but DDP did not significantly inhibit the proliferation of Eca109 / DDP cells (P <0.05) And promote DDP-induced Eca109 / DDP cell cycle changes, increased apoptosis. Cell cycle was significantly increased in G1 phase (P <0.05), S phase cells, G2 phase cells were significantly reduced (P <0.05); apoptosis rate was significantly increased (P <0.05). Conclusion DHA can promote the proliferation of Eca109 / DDP cells induced by DDP, which may be related to the change of the cell cycle and the increase of apoptosis of Eca109 / DDP cells.