摘要
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
Objective To sutdy the pharmaceutic mechanisms of cisplatin, verapamil and SDZ PSC 833, and the mechanism of acquired drug resistance. Methods In two ovarian carcinoma cell lines-one (COC 1) sensitive to cisplatin and one (COC 1/DDP) with acquired drug resistance, the cell growth inhibition rate, apoptotic rate and cell cycle were measured.Results (1) Verapamil or SDZ PSC 833 increased cisplatin cytotoxicity. (2) The cisplatin slowed down the S phase of cell cycle during which the cells under went apoptosis. (3) COC 1 and COC 1/DDP had different apoptotic rates. PSC 833 enhanced COC 1/DDP apoptosis that induced by cisplatin.Conclusion (1) Verapamil and SDZ PSC 833 increase sensitivity to cisplatin, SDZ PSC 833 enhances apoptosis induced by cisplatin. (2) Inducement of apoptosis is one of the pharmaceutic mechanism of cisplatin, acquired drug resistance is associated with apoptosis. (3) The most prominent effect on cell cycle kinetics is a slowdown in S phase, and apoptotic cells are S phase cells.
出处
《肿瘤》
CAS
CSCD
北大核心
2000年第2期93-95,共3页
Tumor
