He Q Y, Zhang H Q, Pang D B, Chi X S, Xue S B
Department of Biology, Beijing Normal University.
Yao Xue Xue Bao. 1996;31(10):721-6.
To further study the relationship between resistance to apoptosis and drug resistance in harringtonine-resistant HL-60 cells (HR20), cyclosporine A (CsA) 20, 10 micrograms.ml-1 was shown to induce the sensitive HL-60 cells to apoptosis, showing a typical DNA "ladder" band. But the same concentrations of CsA retarded the HR20 cells in G1 phase and could not induce the cells to apoptosis. The cellular daunorubicin accumulation increased when HR20 cells were treated with low concentration of CsA and the reversal of drug resistance by CsA was unrelated to the retardation of cell cycle progression. High phosphorylation of about 50 kDa protein occured when HR20 cells were treated with CsA 10 micrograms.ml-1. The results domonstrate that cyclosporine A retarded the harringtonine-resistant HL-60 cells in G1 phase but induced HL-60 cells to apoptosis, and the retardation was unrelated to drug resistance.
为进一步研究高三尖杉酯碱耐药的HL-60细胞(HR20)中抗凋亡与耐药性之间的关系,发现20、10微克/毫升的环孢素A(CsA)可诱导敏感的HL-60细胞凋亡,呈现典型的DNA“梯状”条带。但相同浓度的CsA使HR20细胞阻滞于G1期,不能诱导细胞凋亡。低浓度CsA处理HR20细胞时细胞柔红霉素蓄积增加,且CsA逆转耐药性与细胞周期进程阻滞无关。用10微克/毫升CsA处理HR20细胞时,约50 kDa蛋白出现高度磷酸化。结果表明,环孢素A使高三尖杉酯碱耐药的HL-60细胞阻滞于G1期,但诱导HL-60细胞凋亡,且这种阻滞与耐药性无关。