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三氧化二砷、顺铂对人卵巢癌细胞联合作用研究

Study of Arsenic Trioxide and Cisplatin on Human Ovarian Cancer Cell.
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摘要 目的探讨三氧化二砷(As2O3)、顺铂(DDP)对人卵巢癌细胞HO-8910的联合作用及其相关机制。方法采用形态学方法研究As2O3、DDP对细胞增生的影响,用流式细胞术分析细胞周期,免疫细胞化学染色法检测p53基因表达。结果1.As2O3、DDP协同作用时,浓度分别在1.5μmol/L以上、2μmol/L以上时,有显著性差异;当三氧化二砷、顺铂浓度分别是12μmol/L、4μmol/L时,72h时癌细胞接近100%死亡。2.As2O3、DDP引起HO-8910细胞S期阻滞、p53基因表达增强。结论As2O3、DDP对人卵巢癌细胞HO-8910的生长有协同抑制作用;As2O3、DDP联合作用引起卵巢癌细胞凋亡的机制与S期阻滞、p53基因表达增强有关。 Objective The study was carried out to investigate the effects of arsenic trioxide and cisplatin on ovarian cancer cell line HO - 8910 and relative mechanism. Methods Morphological changes of cells were observed and photoed by inverted microscope. Cell cycle analysis was performed on flow cytometry(FCM). Immunocytochemical staining was used to examine the expression of p53 gene. Results 1. The inhibitive effect of arsenic trioxide ( 〉 1.5μmol/L) combined with cisplatin( 〉 2μmol/L) was obvious and the inhibitive degree was nearly 100% when the concentrations of arsenic trioxide and cisplatin were 12μmol/L and 4μmol/L. 2. Higher concentrations of arsenic trioxide and cisplatin perturbed cell through S - phase and up - regulated p53 gene expressions. Conclusions The inhibitive effect of arsenic trioxide combined with cisplatin was more obvious than either one used separately; the apoptosis mechanism of ovarian cancer cell line HO -8910 is related with perturbing of S phase and up- regulating of p53 gene expression.
出处 《医学研究杂志》 2007年第2期63-65,共3页 Journal of Medical Research
关键词 三氧化二砷(As2O3)顺铂(DDP) 卵巢癌凋亡 Arsenic trioxide Cisplatin Ovarian cancer Apoptosis
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参考文献3

  • 1Mervis J.Ancient remedy perform trick.Science,1996,273(5275):578
  • 2Chen GQ,Zhu J,Shi XY,et al.In vitro studies on cellular and molecular mechanism of arsenic trioxide(As2O3) in the treatment of acute promyelotytic leukemia:As2O3 induces NB4 cell apoptosis with downregulation of bcl-2 expression and modulation of PML-RAR alpha/PML protein.Blood,1996,88(3):1052-1061
  • 3Roboz GJ,DiasS,LamG,et al.Arsenic trioxide induces dose-and time-dependent apoptosis of endothelium and may extert an antileukemic effect via inhibition of angiogenesis.Blood,2000,96(4):1552-1530

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