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目的：寻找克服肿瘤细胞多药耐药的方法。方法：以环孢霉素Ａ（ＣｓＡ）作为耐药逆转剂，用ＭＴＴ法体外药物敏感试验，观察ＣｓＡ对多药耐药白血病细胞株Ｋ５６２／ＤＯＸ的药物敏感性、细胞内药物的积聚和外排的影响。结果：ＣｓＡ可增强阿霉素（ＤＯＸ）对Ｋ５６２／ＤＯＸ的细胞毒作用，且存在剂量依赖关系。ＣｓＡ≥２μｇ／ｍｌ能较明显提高Ｋ５６２／ＤＯＸ对ＤＯＸ的敏感性。用２μｇ／ｍｌＣｓＡ处理后，Ｋ５６２／ＤＯＸ细胞内ＤＯＸ外排速度明显减慢，ＤＯＸ含量仅减少１２．３％，但对Ｋ５６２细胞内药物外排无影响。结论：ＣｓＡ能有效地减慢Ｋ５６２／ＤＯＸ细胞内ＤＯＸ外排速度，增加细胞内ＤＯＸ积聚。ＣｓＡ对Ｋ５６２细胞药物敏感性、细胞内药物外排和积聚均无影响。
Objective: To find a way to overcome the multi-drug resistance of tumor cells. Methods: Cyclosporine A (CsA) was used as drug-resistant reversal agent in vitro drug sensitivity test by MTT method to observe the drug sensitivity of CsA to multidrug-resistant leukemia cell line K562 / DOX, intracellular drug accumulation Row of impact. Results: CsA enhanced the cytotoxicity of doxorubicin (DOX) to K562 / DOX in a dose-dependent manner. CsA≥2μg / ml can significantly improve the sensitivity of K562 / DOX to DOX. After treatment with 2μg / ml CsA, the efflux of DOX in K562 / DOX cells was significantly slowed down, while the DOX content decreased only 12.3%, but had no effect on drug efflux in K562 cells. Conclusion: CsA can effectively slow the efflux of DOX and increase DOX accumulation in K562 / DOX cells. CsA had no effect on K562 cell drug sensitivity, intracellular drug efflux and accumulation.