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目的研究米非司酮对卵巢癌耐药细胞系COC1/DDP的增敏作用及其作用机制。方法用卵巢癌耐药细胞系COC1/DDP和敏感细胞系COC1为实验对象,四甲基偶氮唑蓝(MTT)法检测米非司酮对COC1/DDP细胞的增敏作用,流式细胞仪检测米非司酮对凋亡蛋白Bcl-2、Bax表达的影响。结果1.25μmol/L的米非司酮能够增强COC1/DDP对顺铂的敏感性,并使Bcl-2的阳性率从(23.80±0.44)%下降至(19.40±0.69)%(P=0.000),Bax从(12.75±0.25)%上升至(25.60±0.88)%(P=0.000),其逆转作用有剂量依赖性。结论米非司酮逆转卵巢癌COC1/DDP细胞对顺铂的耐药可能与下调Bcl-2的表达、上调Bax的表达、降低Bcl-2/Bax的比率有关。
Objective To study the sensitizing effect and mechanism of mifepristone on the drug-resistant cell line COC1 / DDP in ovarian cancer. Methods COC1 / DDP and COC1 were used as experimental subjects. MTT assay was used to detect the sensitization effect of mifepristone on COC1 / DDP cells. Flow cytometry To detect the effect of mifepristone on the expression of Bcl-2 and Bax proteins. Results Mifepristone 1.25μmol / L enhanced the sensitivity of COC1 / DDP to cisplatin and decreased the positive rate of Bcl-2 from (23.80 ± 0.44)% to (19.40 ± 0.69)% (P = 0.000) , Bax increased from (12.75 ± 0.25)% to (25.60 ± 0.88)% (P = 0.000), and its reversal effect was dose-dependent. Conclusion Mifepristone reverses the drug resistance of COC1 / DDP cells to cisplatin, which may be related to down-regulating the expression of Bcl-2, up-regulating the expression of Bax and decreasing the ratio of Bcl-2 / Bax.