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阿霉素可导致H9c2心肌细胞中蛋白质多聚(ADP - 核糖基)化的短暂激活。

Doxorubicin causes transient activation of protein poly(ADP-ribosyl)ation in H9c2 cardiomyocytes.

作者信息

Efremova A S, Shram S I, Myasoedov N F

机构信息

Institute of Molecular Genetics, Russian Academy of Sciences, pl. Akademika Kurchatova 46, Moscow, 123182, Russia.

出版信息

Dokl Biochem Biophys. 2015;464:333-7. doi: 10.1134/S1607672915050178. Epub 2015 Oct 31.

DOI:10.1134/S1607672915050178
PMID:26518562
Abstract

Possible involvement of the system of protein poly(ADP-ribosyl)ation in the mechanisms of cardiotoxicity of doxorubicin, one of the most frequently used anticancer drug, was studied in cultures of cardiomyocytes H9c2. The treatment of H9c2 cells with doxorubicin (1 µM) led to a transient (after 6 h of incubation) increase in the nuclear level of poly(ADP-ribosyl)ated proteins. The observed data indirectly indicate the development of genotoxic stress in the doxorubicin-treated cells, probably caused by the stimulatory effects of doxorubicin and its metabolites on the production of reactive oxygen and nitrogen species.

摘要

多柔比星是最常用的抗癌药物之一,在H9c2心肌细胞培养物中研究了蛋白质多聚(ADP - 核糖基)化系统可能参与多柔比星心脏毒性机制的情况。用多柔比星(1μM)处理H9c2细胞导致多聚(ADP - 核糖基)化蛋白的核水平短暂升高(孵育6小时后)。观察到的数据间接表明在多柔比星处理的细胞中发生了基因毒性应激,这可能是由于多柔比星及其代谢产物对活性氧和氮物种产生的刺激作用所致。

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