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目的：在建立体外多药抗药细胞株的基础上，研究其抗药性形成机制，寻求克服抗药性的方法。方法：用人食管癌上皮细胞Eea-109细胞，在无诱导剂的情况下，以递加培养液中阿霉素(ADM)质量浓度的方法，建立了Eca-109／ADM多药抗药细胞株。用荧光光度法测定抗药细胞内还原性谷胱甘肽(GSH)含量及ADM的累积量。结果：研究发现Eca-109／ADM细胞内GSH含量增加、降低细胞内GSH的含量，细胞的抗药性呈现部分逆转；抗药细胞内ADM的质量浓度较敏感株Eca-109细胞低，用维拉帕米能增加抗药细胞内ADM的质量浓度，同时部分逆转其抗药性。结论：Eca-109／ADM细胞的抗药机制主要是由于细胞内GSH含量升高及细胞内药物质量浓度降低所致。“,”Aim: In order to investigate the mechanism of multidrug-resistance in Eca-109/ADM cell line and find ways toreverse resistance to drugs. Methods: Using a multidrug-resistant cell line of Eca-109/ADM established by stepwise selection onexposure to increasing dose of Adriamycin(ADM) in the absence of mutagenic agents, GSH content and ADM accumulation in cellswere determined. Results: GSH content in Eca-109 and Eca-109/ADM cells are (0.32±0.05), (0.69±0.09)ng/106 cells re-spectively. At lowering intracellular GSH content, the drug resistance was only overcome partially. Intracellular ADM accumulationin Eca-109/ADM cells was lower than that in Eca-109 cell. Vempamil in combination with ADM was found to enhance intracellularADM accumulation in Eca-109/ADM cells and brought about the reversion of drug resistance. Conclusion: The mechanism ofEca-109/ADM cell resistance to multiple drug results mainly from increased GSH content and decreased the drug accumulation incells.