PHI逆转K562/A02细胞阿霉素耐药的机制  

Mechanism of phenylhexyl isothiocyanate reversing multidrug resistance to adriamycin in K562/A02 cell line

作　　者：陈宝安[1] 袁鹏[1] 夏国华[1] 程坚[1] 马旭东[2] 刘德龙 鹿全意[4] 

机构地区：[1]东南大学附属中大医院血液病科,南京210009 [2]福建省漳州市医院 [3]Department of Medicine,New York Medical College [4]厦门大学附属中山医院

出　　处：《江苏医药》2010年第10期1164-1167,F0002,共5页Jiangsu Medical Journal

基　　金：国家自然科学基金(39970832;30740062)

摘　　要：目的探讨异硫氰酸苯乙酯(PHI)逆转K562/A02细胞株阿霉素(ADM)耐药的可能机制。方法将耐ADM的人慢性粒细胞白血病K562/A02细胞株分别与不同浓度(0,5,10,20,30,40和50μM)的PHI共同孵育后,流式细胞术检测细胞周期、细胞内ADM浓度以及P-糖蛋白1(P-gp1)表达水平;逆转录聚合酶链反应(RT-PCR)检测PHI作用前后细胞内mdrl mRNA的转录水平。结果与对照组相比,联合作用48h后,随着PHI浓度的增加G2期细胞逐渐减少,G1期细胞明显增多,而S期细胞无明显变化;K562/A02细胞内ADM平均荧光强度均高于对照组;K562/A02细胞mdrl mRNA表达下降和P-gp1表达下调(P<0.05)。结论 PHI逆转K562/A02细胞耐药机制可能与细胞G1期阻滞和P-gp1表达下调有关。Objective To elucidate the mechanism of phenylhexyl isothiocyanate （PHI） on the reversal of K562/A02 cell line.Methods After adriamycin（ADM） resistant K562/A02 cells were incubated with different concentrations of PHI（5,10,20,30,40 and 50 μM） or without PHI （control）,flow cytometry（FCM）was used to evaluate cell cycle distributions,intracellular concentration of ADM,and the expression of P-gp1,respectively.Furthermore,mdrl mRNA was detected by reverse transcription polymerase chain reaction（RT-PCR） assay before and after use of PHI.Results The number of K562/A02 cells of G2 phase decreased and G1 phase increased,while the S phase had no obvious changes.The intracellular concentrations of ADM in K562/A02 cells were all higher than those in control groups.The transcription of mdrl mRNA and expression of P-gp1 were decreased and down-regulated with the increase of PHI,respectively （P0.05） when compared to those of control groups.Conclusion Multidrug resistance of K562/A02 can be partly reversed by PHI,which may be related to the arrest of G1 and the decrease of P-gp1 expression.

关 键 词：异硫氰酸苯乙酯 K562/A02细胞 耐药逆转 

分 类 号：R733[医药卫生—肿瘤]