摘要
目的 :研究异搏定对 P-糖蛋白 (Pgp)介导的人类白血病 K 5 6 2细胞多药耐药作用。方法 :用台盼蓝拒染法检测药物敏感性及异搏定对细胞耐药性的影响 ,用免疫组织化学法检测 Pgp的表达 ,用流式细胞仪检测细胞内柔红霉素 (DNR)积聚。结果 :DNR诱导的耐药细胞 K5 6 2 / D对 DNR、长春新碱 (VCR)、高三尖杉脂碱 (HHT)、鬼臼乙叉甙 (VP16 )、米托恩醌 (MIT)交叉耐药。 DNR诱导了 K5 6 2 / D细胞的 Pgp过度表达。异搏定使 K 5 6 2 / D细胞内药物积聚增加 ,明显地逆转了 K5 6 2 / D细胞对 DNR、VCR、MIT、HHT、VP- 16的耐药性 ,而对敏感细胞 K5 6 2 / S的耐药性无影响。结论 :DNR诱导了 K5 6 2 / D细胞的 Pgp过度表达 ,异搏定通过抑制 Pgp功能逆转了 Pgp介导的K5 6 2 /
Objective: This test was designed to study the effects of verapamil on P glycoprotein (Pgp) mediated multidrug resistance (MDR) in human leukemia K562 cells. Methods: Trypanblue dye exclusion method was used to observe the drug sensitivity and the effect of verapamil on the drug resistance; immunohistochemical technique to analyze Pgp phenotype, and flow cytometer was used to measure the intracellular drug accumulation. Results: Resistant cells (K562/D) induced by DNR were cross resistant to DNR, HHT, VP16 and MIT. DNR induced overexpression of Pgp in K562/D cells; Verapamil increased the intracellular drug accumulation, and then obviously reversed the drug resistance to DNR, VCR, MIT, HHT, and VP 16 in K562/D cells, but not in the sensitive cells (K562/S). Conclusion: The multidrug resistance of K562/D cells can be induced by DNR which is related to the Pgp overexpression, and verapamil reversed the DNR resistance by increasing the intracellular accumulation of DNR.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2000年第3期189-191,共3页
Journal of China Medical University
基金
辽宁省自然科学基金!962 3 03
