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目的探讨低剂量拓扑替康(TPT)治疗肺癌脑转移的机制。方法采用体外培养耐顺铂肺腺癌细胞HTB-56/DDP,并用Annexin V-FITC染色法检测细胞的早期凋亡;PI单染色法检测细胞周期。结果 Caspase-3、8特异性抑制剂和TPT联用组与单用TPT组相比其存活率较高(P<0.05);TPT组(6.4μmol.L-1)于12h出现早期凋亡,caspase抑制剂组出现延迟,凋亡率降低;流式细胞仪检测到细胞周期发生改变,G1期细胞较对照组增多(P<0.05),S期细胞减少(P<0.05)。结论低剂量TPT治疗肺癌脑转移的机制可能与其诱导肿瘤细胞凋亡相关,该过程与caspase-3、8的相关活化过程有关。
Objective To investigate the mechanism of low-dose topotecan (TPT) on brain metastasis of lung cancer. Methods To investigate the cell cycle and early apoptosis of A549 cells treated with cisplatin-resistant lung adenocarcinoma cell line HTB-56 / DDP by Annexin V-FITC staining. Results The survival rate of Caspase-3, 8-specific inhibitor and TPT combined group was higher than that of TPT group (P <0.05). Early apoptosis of TPT group (6.4μmol.L-1) In the caspase inhibitor group, the apoptosis rate was decreased. The cell cycle was detected by flow cytometry. The number of cells in G1 phase increased compared with that in control group (P <0.05) and decreased in S phase (P <0.05). Conclusion The mechanism of low-dose TPT in the treatment of brain metastasis of lung cancer may be related to the apoptosis of tumor cells induced by TPT. The process is related to the activation of caspase-3 and 8.