汉防己甲素逆转白血病细胞株K562/ADM多药耐药性机制研究  

Reversal Mechanism of Multidrug Resistance in Leukemia Cell Line K562/ADM

作　　者：许文林[1] 江云伟[1] 王法春[1] 袁伟[1] 林江[1] 阮长耿[2] 

机构地区：[1]江苏省镇江市第一人民医院,212002 [2]苏州大学附属第一医院,300020

出　　处：《实用癌症杂志》2003年第4期347-349,共3页The Practical Journal of Cancer

摘　　要：目的　研究汉防己甲素 (TTD)对慢性粒细胞白血病急性变白血病细胞株K 5 62 /ADM多药耐药 (MDR )逆转的机理。方法　采用流式细胞仪检测细胞内化疗药物的浓度及细胞表面P糖蛋白 (P -gp)的表达 ;荧光定量PCR法检测MDR1mRNA ;通过流式细胞仪检测Anexin -V判断凋亡细胞的数量。结果　 10 μmol/L的TTD处理K 5 62 /ADM细胞后 ,细胞内阿霉素 (ADM )的浓度明显提高 ;K 5 62 /ADM细胞MDR 1mRNA /P -gp的表达下降 ;TTD能增强ADM致细胞凋亡的作用。 结论　汉防己甲素的耐药逆转机制除了下调MDR 1mRNA /P -gp的表达引起细胞内抗癌药物的积聚外 。Objective To investigate the reversal mechanism of Tetredrine(TTD) on multidrug resistance in leukemia cell line K562/ADM.Methods Using flow cytometry(FCM) assay,the intracellular ADM concentration and the expression of P-glycoprotein(P-gp) were examined.The mRNA expressions of multidrug resistance(MDR) was measured by fluorescent quantitative reverse transcriptase polymerase chain reaction(RT-PCR).Apoptotic changes were observed by Anexin-V.Results 10 μmol/L TTD significantly increased the intracellular concentration of ADM and reduced the expression of MDR1 mRNA/P-gp in K562/ADM cells.TTD can effectively enhanced the effect of ADM on apoptosis of K562/ADM cells.Conclusion The reversal mechanism of multidrug resistance in K562/ADM takes place through different ways,such as down-regulating mRNA and protein expression levels of MDR1,increasing intracellular drug concentration,and raising the number of apoptosis cells.

关 键 词：白血病 K562/ADM细胞 汉防己甲素 多药耐药性 P糖蛋白 

分 类 号：R733.7[医药卫生—肿瘤]