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近几年对喹啉类抗疟药作用方式的研究进展甚微。现有的资料否定了以往对这类药物作用机制的设想。本文概述了一个新的药物作用靶,体外观察表明这类药物能阻止宿主细胞释放铁,从而影响疟原虫生长所需要的铁质的供应。抗喹啉类药疟原虫其酸性食物泡内聚积的药物浓度较低。动力学模型表明这一现象并不是多药抗性(MDR)泵作用的结果而是食物泡上质子泵活力降低所致。疟原虫mdr基因分子生物学研究表明基因表达或变异与药物抗性表型间并无相关性。一些可逆转MDR癌细胞的化合物可逆转疟原虫抗药性,其机制似乎不同于癌细胞中MDR泵的作用。
In recent years, research on the mode of action of quinoline antimalarial drugs has been made little progress. The available information denies the previous assumption of the mechanism of action of such drugs. This article outlines a new drug target that has been shown in vitro to show that such drugs prevent iron release from host cells and thus affect the supply of iron needed for Plasmodium growth. Anti-quinoline drugs Plasmodium acid food bubble accumulation of drug concentration is low. The kinetic model shows that this phenomenon is not the result of the multidrug resistance (MDR) pump action but rather the reduced viability of the proton-pump food. Molecular biology of mdr gene in Plasmodium showed no correlation between gene expression or mutation and drug resistance phenotype. Some compounds that reverse MDR cancer cells can reverse Plasmodium resistance, the mechanism of which seems to differ from that of MDR pumps in cancer cells.