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Arsenic trioxide inhibits P-glycoprotein expression in multidrug-resistant human leukemia K562/ADM cell line that overexpresses mdr-1 gene and enhances their chemotherapeutic sensitivity
Author(s): 
Pages: 28-31
Year: Issue:  1
Journal: CHINESE JOURNAL OF HEMATOLOGY

Keyword:  砷剂药物疗法抗药性多药P糖蛋白细胞凋亡药物协同作用;
Abstract: 目的研究三氧化二砷(As2O3)对人多药耐药白血病细胞K562/ADM的诱导凋亡作用和对P-糖蛋白(P-gp)表达及功能的影响,以及As2O3与常规化疗药物对耐药细胞的联合效应. 方法以白血病多药耐药细胞系K562/ADM为As2O3作用的靶细胞,用MTT比色法检测细胞增殖活性,光镜、激光共聚焦显微镜和电镜观察形态学变化,流式细胞术进行细胞周期分析和P-gp表达的检测,激光共聚焦显微镜检测P-gp功能.结果 K562/ADM 细胞对阿霉素(ADM)高度耐受,并与柔红霉素(DNR)和足叶乙甙(Vp16)交叉耐药.0.5~20.0 μmol/L As2O3抑制K562/ADM细胞增殖,抑制活性高于K562细胞.经As2O3诱导后K562/ADM细胞出现典型的凋亡形态学变化和亚G1期细胞比例增高等凋亡特征性改变.As2O3下调K562/ADM细胞P-gp的表达并抑制其功能,增加K562/ADM细胞对ADM、DNR和Vp16的敏感性.结论 As2O3能够诱导白血病多药耐药细胞凋亡,并通过抑制耐药细胞P-gp的表达和功能提高耐药白血病细胞对常规化疗药物的敏感性.
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