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机构地区:[1]海南工商职业学院应用技术系,海口570203 [2]海口经济学院工程技术学院,海口570203
出 处:《生物技术通报》2013年第2期177-183,共7页Biotechnology Bulletin
摘 要:旨在研究福安泰(FAT)对人类白血病K562/A02细胞多药耐药的逆转作用。用噻唑蓝(MTT)法检测药物敏感性及FAT对细胞耐药性的影响;用流式细胞仪检测细胞内罗丹明123(Rhodamine 123)的含量;采用生物化学DTNB法测定细胞内GSH含量。结果显示,低浓度FAT对K562/A02细胞和K562细胞均无直接细胞毒作用。FAT可以降低阿霉素对K562/A02细胞的IC50值,对K562细胞没有明显影响。FAT可增加K562/A02细胞内罗丹明123(Rhodamine 123)的含量。K562/A02细胞内GSH含量高于K562细胞内GSH含量,FAT可降低K562/A02细胞内GSH的含量。表明FAT降低K562/A02细胞内GSH的含量是FAT逆转MDR的机制之一。This test was designed to study the effects of FAT on muhidrug resistance ( MDR ) in human leukemia K562/A02 cells. M33' method was used to observe the drug sensitivity and the effect of FAT on the drug resistance ; Flow cytometer was used to measure the intracellular drug accumulation ; Cellular GSH concentration was examined by biochemical analyses with DTNB. Results showed that FAT did not exhibit an inhibitory activity to proliferation in K562 call line and K562/A02 cell line. FAT decreased ICs0 of ADM in K562/A02 cell line. And it had no remarkable effect on K562 cell line. FAT increased the intracellular Rho-123 concentration. Cellular GSH concentration in K562/ A02 cell line was higher than thatin K562 cell line. FAT decreased cellular GSH concentration in K562/A02 cell line. One of the mechanisms of multidrug resistance reversal by FAT was decrease of cellular GSH concentration in K562/A02 call line.
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