顺铂及增敏剂Verapamil、SDZ PSC 833诱导卵巢癌细胞凋亡的研究

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目的 探讨顺铂及 Verapam il、SDZ PSC 833作用机制 ,探讨获得性耐药机制。方法 以人卵巢癌亲代细胞株COC1 及其耐药亚株 COC1 /DDP为材料 ,计算细胞生长抑制率、细胞凋亡率及进行细胞周期分析。结果 顺铂联用Verapamil或 SDZ PSC833可提高细胞生长抑制率 ;顺铂引起 S期细胞比例增高 ,大剂量顺铂造成 S期细胞大量凋亡 ;COC1 、COC1 /DDP凋亡率不同 ,PSC833能明显增强顺铂诱导 COC1 /DDP细胞凋亡。结论  Verapamil、PSC833有增敏作用 ,PSC833能增强顺铂诱导 COC1 /DDP细胞凋亡 ;诱导细胞凋亡是顺铂作用机制之一 ,获得性耐药与凋亡耐受有关 ;顺铂引起 S期细胞增多 ,凋亡细胞为 S期细胞 Objective To investigate the mechanism of action of cisplatin and Verapam il SDZ PSC 833 to explore the mechanism of acquired resistance. Methods The human ovarian cancer cell line COC1 and its drug-resistant sub-strain COC1 / DDP were used as materials to calculate the cell growth inhibition rate and apoptosis rate and to conduct cell cycle analysis. Results Cisplatin combined with Verapamil or SDZ PSC833 increased the rate of cell growth inhibition. Cisplatin induced an increase in the proportion of cells in S phase and a large dose of Cisplatin resulted in a large number of apoptotic cells in S phase. The apoptotic rates of COC1 and COC1 / DDP were different, and PSC833 was significantly Enhance cisplatin-induced COC1 / DDP cell apoptosis. Conclusions Verapamil and PSC833 have sensitization effect. PSC833 can enhance cisplatin-induced apoptosis of COC1 / DDP cells. Inducing apoptosis is one of the mechanisms of cisplatin. Acquired resistance is related to apoptosis tolerance. Cisplatin causes S phase Cells increased, apoptotic cells S phase cells
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