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通过体外转染多药耐受相关蛋白 (MRP)基因和化疗药物 VP- 16、 5 - Fu诱导的方法分别建立了膀胱癌多药耐受 (MDR)细胞亚系 EJ/ MRP和鼻咽癌 MDR亚系 L CE/ VP、L CE/ Fu,并观察了细胞因子 rh G- CSF、IFN- α1b和 IL-2对这些亚系 MDR水平的影响。结果发现 IFNα1b和 IL- 2可以一定程度地逆转 3种 MDR细胞对 VP- 16耐受程度 ,逆转倍数在 3.4与 5 .2之间 ,可以增加柔红霉素 Dau在 MDR细胞内的聚集程度 ;相反地 ,rh G- CSF增强了 MDR细胞对VP- 16的耐受程度和降低了 Dau的胞内聚集程度。以上揭示 IFNα1b、IL- 2对 P- gp或 (和 ) MRP介导的 MDR具有逆转作用 ,rh G- CSF则增强了 P- gp或 (和 ) MRP介导的 MDR程度 ,这为 MDR研究和临床癌症治疗提供了一定参考
Multidrug resistance (MDR) cell subline EJ/MRP and nasopharyngeal carcinoma MDR were established by in vitro transfection of multidrug resistance-associated protein (MRP) gene and chemotherapeutic drug VP-16,5-Fu. The subfamily L CE/VP, L CE/Fu, and the effects of the cytokines rh G-CSF, IFN-α1b, and IL-2 on the MDR levels of these sublines were observed. The results showed that IFNα1b and IL-2 could reverse the tolerance of VP-16 in three kinds of MDR cells to a certain extent. The reversal multiples were between 3.4 and 5.2, which increased the degree of aggregation of daunorubicin Dau in MDR cells. In contrast, rh G-CSF enhanced the tolerance of MDR cells to VP-16 and decreased the intracellular aggregation of Dau. The above revealed that IFNα1b, IL-2 had a reversal effect on P-gp or (and) MRP-mediated MDR, and rh G-CSF enhanced P-gp or (and) MRP-mediated MDR, which was the study of MDR and Clinical cancer treatment provides some reference