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目的：研究维拉帕米逆转肿瘤多药抗药性的作用及机理。方法：ＭＴＴ法测药敏；用流式细胞仪测细胞对罗丹明１２３的蓄积、外排及耐药蛋白的表达。结果：耐药株的耐药性是亲本株的１７２倍；维拉帕米使耐药株的ＩＣ５０逆转了２～７９倍。耐药株表达耐药蛋白，亲本株为阴性；维拉帕米不影响耐药蛋白的表达。耐药株与亲本株相比，罗丹明的蓄积减少、外排加速；维拉帕米使耐药株的外排显著延缓。结论：维拉帕米能通过调节耐药蛋白的功能显著地逆转ＫＢｖ２００的多药抗药性，而不影响耐药蛋白的表达
Objective: To study the effect and mechanism of verapamil on reversing multidrug resistance of tumor. Methods: MTT assay was used to measure the drug sensitivity. Flow cytometry was used to measure the accumulation of rhodamine 123, efflux and expression of drug resistance protein. Results: The resistance of the resistant strains was 172 times that of the parent strain; verapamil reversed the IC50 of the resistant strains by 2 to 79 times. The resistant strains expressed the resistant protein and the parent strain was negative. Verapamil did not affect the expression of the resistant protein. Compared with the parental strains, the resistance of rhodamine decreased and the exocytosis accelerated. The verapamil delayed the efflux of drug-resistant strains. CONCLUSION: Verapamil significantly reverses the multidrug resistance of KBv200 by regulating the function of the resistant protein without affecting the expression of the resistant protein