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目的:探讨米非司酮(mifepristone)联合三氧化二砷(As2O3)对K562/ADM的逆转作用及机制研究。方法:不同浓度米非司酮、As2O3处理细胞72h,采用MTT法检测细胞增殖活性;流式细胞仪检测细胞凋亡、分光光度法检测细胞谷胱甘肽(GSH)含量。结果:10μmol.L-1的米非司酮对K562/ADM细胞无明显杀伤,可有效逆转K562/ADM细胞耐药性,此浓度米非司酮联合As2O3(2.0μmol.L-1)作用于K562/ADM细胞后,逆转倍数明显增高(P<0.01),GSH含量明显低于同浓度单用药组(P<0.05)。对细胞增殖抑制及其诱导凋亡的效果均明显高于同浓度单用药组(P<0.05)。结论:米非司酮联合As2O3逆转作用增强,机制可能与凋亡加强及GSH含量改变有关。
Objective: To investigate the reversal effect of mifepristone and arsenic trioxide (As2O3) on K562 / ADM and its mechanism. Methods: The cells were treated with different concentrations of mifepristone and As2O3 for 72 hours. Cell proliferation was measured by MTT assay. Apoptosis was detected by flow cytometry. The content of glutathione (GSH) was detected by spectrophotometry. Results: Mifepristone (10μmol.L-1) had no obvious killing effect on K562 / ADM cells, which could effectively reverse the drug resistance of K562 / ADM cells. Mifepristone and As2O3 (2.0μmol.L-1) K562 / ADM cells, the reversal fold was significantly increased (P <0.01), GSH content was significantly lower than the same concentration of single-agent group (P <0.05). The inhibitory effect on cell proliferation and the induction of apoptosis were significantly higher than those of the single drug group (P <0.05). Conclusion: The reversal effect of mifepristone combined with As2O3 is enhanced. The mechanism may be related to the enhancement of apoptosis and the change of GSH content.