维拉帕米对诱导耐药白血病P388细胞中阿霉素积累的影响。

Archiv fur Geschwulstforschung Pub Date : 1990-01-01
L V Moroz, F V Donenko, N B Borovkova, S M Sitdikova
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引用次数: 0

摘要

利用小鼠BDF1研究表明,与对Dx敏感的P388细胞相比,在诱导抗生素耐药(P388/Dx)的白血病P388细胞中,多柔比星(Dx)的滞留时间更短。在240 min的观察期内,维拉帕米(Vp)可导致白血病P388/Dx细胞中Dx浓度升高。Vp能促进Dx对P388/Dx小鼠的治疗作用。由于Vp不改变抗生素在小鼠血浆中的循环周期,因此可以认为Vp的作用机制是在诱导耐药的细胞中清除受损的Dx。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Verapamil effect on the accumulation of doxorubicin in the leukemia P388 cells with induced antibiotic resistance.

Using mice BDF1 it has been shown that the period of retention of Doxorubicin (Dx) is shorter in the leukemia P388 cells with induced antibiotic resistance (P388/Dx) as compared to P388 cells sensitive to Dx. Administration of Verapamil (Vp) to animals leads to an increase of Dx concentration in the leukemia P388/Dx cells during a 240 min observation period. Vp promotes the therapeutic effect of Dx on P388/Dx bearing mice. It can be suggested that the mechanism of Vp action consists in the damaged Dx elimination from cells with induced resistance, since Vp doesn't change the period of circulation of the antibiotic in the blood plasma of mice.

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