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目的:探讨磷脂酰肌醇3-激酶(phosphatidylinositol 3-kinase,PI3K)抑制剂LY294002(LY)和wortmannin(Wort)对米托蒽醌(mitoxantrone,MIT)耐药的人乳腺癌细胞株MCF-7/MIT耐药性的逆转作用。方法:LY或Wort与MIT联合作用耐药细胞株MCF-7/MIT后,在光学显微镜下记录细胞生长状况,MTT法检测细胞增殖和细胞活性。FCM法检测细胞内MIT的积聚。罗丹明123(rhodamine 123,Rh123)染色法检测细胞线粒体膜电位。碘化丙啶(propidium iodide,PI)染色法检测细胞周期。结果:LY和MIT联合作用可显著增强MIT引起的MCF-7/MIT细胞增殖抑制作用、由MIT引起的线粒体膜电位下降以及细胞周期S和G2/M期阻滞,其作用机制与LY增加MIT在MCF-7/MIT细胞内的积聚有关;Wort对MIT的药效无明显增强作用。结论:LY和MIT联合作用可显著提高耐药细胞株MCF-7/MIT对MIT的敏感度。
Objective: To investigate the effects of phosphatidylinositol 3-kinase (PI3K) inhibitors LY294002 (LY) and wortmannin (Wort) on human breast cancer cell line MCF-7 resistant to mitoxantrone / MIT reversal of drug resistance. Methods: After LY or Wort and MIT combined with drug-resistant cell line MCF-7 / MIT, cell growth was recorded under optical microscope. Cell proliferation and cell viability were detected by MTT assay. FCM method to detect intracellular accumulation of MIT. Rhodamine 123 (Rh123) staining was used to detect mitochondrial membrane potential. Propidium iodide (PI) staining was used to detect cell cycle. Results: The combination of LY and MIT could significantly enhance the inhibitory effect of MIT on the proliferation of MCF-7 / MIT cells, the decrease of mitochondrial membrane potential induced by MIT and the arrest of cell cycle S and G2 / M phases. In MCF-7 / MIT cells accumulation; Wort MIT efficacy was not significantly enhanced. Conclusion: The combination of LY and MIT can significantly improve the sensitivity of multidrug resistant cell line MCF-7 / MIT to MIT.