异喹啉类的新化合物CPUC1对K562/A02细胞多药耐药的逆转作用  

Effect of a novel isoquinoline derivative,CPUC1 on the reversal of multidrug resistance in K562/A02 cells

作　　者：后媛媛[1] 祝浩杰[1] 何玲[1] 刘国卿[1] 

机构地区：[1]中国药科大学药理学教研室,江苏南京210009

出　　处：《中国药理学通报》2004年第8期886-889,共4页Chinese Pharmacological Bulletin

摘　　要：目的　研究新化合物CPUC1对K5 6 2 /A0 2细胞多药耐药的逆转作用。方法　MTT法检测长春新碱细胞毒作用。流式细胞仪测定细胞内罗丹明 12 3的累积。DNA含量分析和AnnexinV/PI双染测定长春新碱诱导的细胞凋亡作用。结果　CPUC1可以明显逆转K5 6 2 /A0 2细胞对长春新碱的耐药性。CPUC1可以浓度依赖性增加K5 6 2 /A0 2细胞内罗丹明12 3的积累。CPUC1可明显增强长春新碱诱导的K5 6 2 /A0 2细胞凋亡。结论　CPUC1通过抑制P 糖蛋白 (P glycoprotein ,P gp)功能逆转了P gp介导的K5 6 2 /A0Aim To study the reversal effect of CPUC1 on multidrug resistance in K562/A02 cells. Methods MTT assay was used to detect the cytotoxicity of vincristine. Intracellular accumulation of rhodamine123 was measured by flow cytometry to evaluate the function of P glycoprotein(Pgp). The apoptotic cells induced by vincristine were detected by flow cytometry using DNA content analysis and Annexin V/PI double staining. Results CPUC1 significantly reversed the resistance of K562/A02 cells to vincristine. CPUC1 increased intracellular accumulation of rhodamine123 in K562/A02 cells in a concentration dependent manner. CPUC1 increased the apoptosis induced by vincristine. Conclusion CPUC1 reversed multidrug resistance by inhibiting function of P gp in K562/A02 cells, suggesting that CPUC1 merits further study.

关 键 词：多药耐药性 细胞凋亡 异喹啉 CPUC1 

分 类 号：R329.25[医药卫生—人体解剖和组织胚胎学] R978.61[医药卫生—基础医学]