目的探讨五味子乙素(SchB)对转染多药耐药1基因(MDR1)的人乳腺癌细胞MCF7的多药耐药逆转作用及相关机制。方法将人MDR1基因导入MCF7细胞,形成耐药细胞株MCF7/MDR1;用该细胞株为模型评价SchB的体外逆转多药耐药作用,用MTT法进行化疗药物单独或与SchB联合作用时对耐药细胞的IC50比较,计算逆转倍数。结果转染细胞MCF7/MDR表现为P糖蛋白高表达,对阿霉素、长春新碱、紫杉醇、高三尖杉酯的抗药性均增加;SchB(25μmol/L)显著减少阿霉素、长春新碱、紫杉醇和高三尖杉酯对MCF7/MDR细胞的IC50,逆转倍数达6.03～23.94倍;SchB(25μmol/L)使MCF7/MDR细胞对若丹明123的胞内积聚增加约5倍,效果与维拉帕米10μmol/L浓度时相当;但SchB(25μmol/L)不影响MCF7/MDR细胞的P糖蛋白表达。结论SchB能有效逆转转染MDR1的MCF7细胞的多药耐药,其机制可能是抑制了P糖蛋白的药物外排生物学活性。 Objective To investigate the reversal effect and mechanism of Schisandrin B (SchB) on multidrug resistance of human breast cancer cell MCF7 transfected with multidrug resistance 1 gene (MDR1). Methods Human MDR1 gene was introduced into MCF7 cells to form a resistant cell line MCF7/MDR1. Schl was used as a model to evaluate the reversal of multidrug resistance in vitro. MTT method was used to treat chemotherapeutic drugs alone or in combination with SchB. The IC50 of drug cells was compared and the fold reverse was calculated. Results The MCF7/MDR transfected cells showed high expression of P-glycoprotein, the drug resistance to adriamycin, vincristine, paclitaxel and homoharringtonine increased; SchB (25 μmol/L) significantly reduced doxorubicin and Changchunxin. The IC50 of the base, paclitaxel, and homoharringtonine on MCF7/MDR cells was 6.03-23.94 fold. The SchB (25 μmol/L) increased the intracellular accumulation of rhodamine 123 in MCF7/MDR cells by about 5-fold. It was comparable to verapamil 10 μmol/L; however, SchB (25 μmol/L) did not affect the expression of P-glycoprotein in MCF7/MDR cells. Conclusion SchB can effectively reverse multidrug resistance of MCF7 cells transfected with MDR1. The mechanism may be that it inhibits the biological activity of P glycoprotein.