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顺铂 维拉帕米和环孢菌素诱导卵巢癌细胞凋亡的研究

廖美焱  陈惠祯  水华  胡杰  杨庆忆  邱慧玲  陈红

摘 要:目的 探讨顺铂(DDP)、维拉帕米(VP)及3′-酮基-去甲基苏氨酸1-缬氨酸2-环孢菌素(PSC 833)诱导卵巢癌细胞凋亡的作用机理。方法 以人卵巢癌亲代细胞株 COC1及其耐DDP亚细胞株COC1/DDP为材料,根据所加药物的不同分为DDP组、VP组、PSC 833组、DDP联合VP组、DDP联合PSC 833组和对照组,计算各组细胞生长抑制率、细胞凋亡率同时进行细胞周期分析。结果 DDP联合VP组和DDP联合PSC 833组COC1、COC1/DDP的细胞生长抑制率均增高,两组COC1的细胞生长抑制率分别为48.56%和47.86%、两组COC1/DDP的细胞生长抑制率分别为39.47%和37.81%,量效曲线均下移,两组分别与DDP组比较,差异均有显著性(P<0.05)。DDP引起S期细胞比例增高,当DDP浓度为1.0 μg/ml时,COC1 细胞S期比例最高达99.67%,而DDP浓度为2.0 μg/ml时,S期比例最低降至33.61%,S期细胞大量凋亡;COC1、COC1/DDP的细胞凋亡率不同,DDP(0.5~2.0 μg/ml)+PSC 833(0.30 μg/ml)时的细胞凋亡率明显提高,与对照组比较,差异均有显著性(P均<0.05)。结论 VP、PSC 833有增敏作用,PSC 833能增强DDP诱导COC1/DDP细胞凋亡的作用。诱导细胞凋亡是DDP作用于COC1、COC1/DDP细胞的机理之一,获得性耐药与细胞凋亡耐受有关。
关键词:卵巢肿瘤; 脱噬作用; 抗药性;  顺铂; 维拉帕米

Apotosis Induced by Cisplatin and Verapamil or SDZ PSC 833 in Human Ovarian Cell Lines

LIAO Meiyan CHEN Huizhen SHUI Hua et al
(Department of Oncology, Second Affiliated Hospital,Hubei Medical University,Wuhan 430071, China)

Abstract:Objective To study the pharmaceutical mechanisms of cisplatin(DDP), verapamil(VP) and SDZ PSC833, and the mechanism of developing acquired drug resistance. Methods Two ovarian carcinoma cell lines——one sensitive (COC1) and the other resistant (COC1/DDP) to cisplatin were used in this study. The cell viability was measured by trypan blue dye exclusion assay. The apopotic cells were observed and distinguished by light and electron microscopy, and comet assay. Flow cytometry was used to measure the cell cycle. Six groups were set up according to drug(s) delivered: DDP, VP, SDZ PSC833, DDP and VP, DDP and SDZ PSC833, and control group. Results (1) VP or SDZ PSC833 enhanced cytotoxicity of DDP (q>1, P<0.01). (2)The most prominent effect of DDP on cell cycle kinetics was a slowdown in S-phase transit during which cells undergo apoptosis (P<0.05). (3) COC1 and COC1/DDP cells had different rates of apoptosis when DDP added. SDZ PSC833

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