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目的:探讨atemoyacin-B(Ate)克服肿瘤多药抗药性(MDR)作用及其机制,方法:Bullatacin(Bul)为阳性对照物,细胞毒测定以MTT法;P-gp功能测定以Fura 2-AM法;细胞内药物积累测定以荧光分光光度计法;细胞凋亡测定以流式细胞仪法,结果:Ate对MCF-7/Dox,MCF-7,KBvzoo和KB细胞的IC_(50)分别为122,120,1.34,1.27 nmol·L~(-1),Ate显著增加MDR细胞内Fura-2及多柔比星(Dox)的积累,但不增加相应敏感细胞的细胞内Fura-2及Dox的积累,Ate也能诱导MDR细胞凋亡.结论:MDR细胞对Ate同样敏感,不受抗药性影响,其机制与降低P-gp功能及增加细胞内药物积累有关。
Objective:To investigate the effect of atemoyacin-B (Ate) on overcoming drug multidrug resistance (MDR) and its mechanism. Methods: Bullatacin (Bul) as positive control, cytotoxicity assay with MTT assay, and P-gp assay with Fura 2- AM method; Intracellular drug accumulation assay by fluorescence spectrophotometry; Apoptosis assay by flow cytometry method Results: Ate IC50 for MCF-7/Dox, MCF-7, KBvzoo, and KB cells At 122, 120, 1.34 and 1.27 nmol·L -1 , Ate significantly increased the accumulation of Fura-2 and Doxorubicin (Dox) in MDR cells, but did not increase the intracellular Fura-2 and Dox of the corresponding sensitive cells. Accumulation of Ate can also induce apoptosis in MDR cells. Conclusion: MDR cells are equally sensitive to Ate and are not affected by drug resistance. The mechanism is related to the decrease of P-gp function and increase of intracellular drug accumulation.