雷公藤甲素对K562/A02细胞阿霉素敏感性的影响  

Effect of Triptolide on Sensitivity of K562/A02 Cell Line to Adriamycin

作　　者：惠璐璐[1] 许文林[1] 陈巧云[1] 朱小兰[1] 龙璐璐[1] 徐颖[1] 秦蓉[1] 

机构地区：[1]江苏大学附属人民医院中心实验室,江苏镇江212002

出　　处：《中国实验血液学杂志》2012年第1期66-69,共4页Journal of Experimental Hematology

基　　金：国家自然科学基金(编号81070423);江苏省医学重点人才资助项目(编号RC2007034)

摘　　要：本研究旨在探讨雷公藤甲素(TPL)对K562/A02细胞阿霉素敏感性的影响。采用MTT法检测TPL细胞毒性和阿霉素药物敏感性;流式细胞术检测P-糖蛋白表达和细胞内阿霉素浓度;双荧光素酶报告基因系统检测MDR1启动子活性。结果表明:TPL增强K562/A02细胞阿霉素敏感性。TPL作用后,K562/A02细胞P-糖蛋白表达相关平均荧光强度(MFI)由123±13下降到39±13(P<0.05);K562/A02细胞内阿霉素相关MFI由18±5上升到34±6(P<0.05),TPL能够有效抑制K562/A02细胞的药物外排。TPL降低MDR1启动子转录活性约75%。结论:TPL通过下调P-糖蛋白表达增强K562/A02细胞对阿霉素的敏感性,其有可能成为一种耐药逆转剂。This study was aimed to evaluate the effect of triptolide （TPL） on the reversal of multidrug resistance in K562/A02 cell line. The sensitivity of K562 and K562/A02 to adriamycin （ADM） and reversal of drug resistance were determined with MTI method. The concentration of intracellular ADM and P-glycoprotein expression were detected by flow cytometry. Luciferase reporter gene assay was used to detect the transcriptional activity of MDR1 promoter. The results showed that TPL significantly decreased the resistance degree of K562/A02 cells, inhibited P-glycoprotein expression （mean fluorescent intensity decreased from 123 ± 13 to 39 ± 13） and increased the intracelluar concentration of ADM （mean fluorescent intensity increased from 18±5 to 34 ± 6） in K562/A02 ceils. Luciferase reporter gene assay demonstrated that TPL inhibited the transcriptional activity of MDR1 promoter by 75%. It is concluded that TPL may effectively reverse the multidrug resistance in K562/A02 cells via modulating P-glycoprotein expression and increasing intracellular ADM accumulation.

关 键 词：雷公藤甲素 K562/A02细胞株 阿霉素 多药耐药 

分 类 号：R733.7[医药卫生—肿瘤] R979.1[医药卫生—临床医学]