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右丙亚胺对表柔比星致大鼠心肌损伤的保护作用及机制研究

吴晖 欧阳取长 刘莉萍 鲁军 水峥嵘

肿瘤药学Issue(1):40-45,6.
肿瘤药学Issue(1):40-45,6.DOI:10.3969/j.issn.2095-1264.2014.008

右丙亚胺对表柔比星致大鼠心肌损伤的保护作用及机制研究

Effects of Dexrazoxane on Pharmorubicin Induced Myocardial Damage and its Mechanisms

吴晖 1欧阳取长 1刘莉萍 1鲁军 1水峥嵘1

作者信息

  • 1. 湖南省肿瘤医院/中南大学湘雅医学院附属肿瘤医院 乳腺内科,湖南 长沙,410013
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摘要

Abstract

Objective To explore the effects of dexrazoxane on pharmorubicin induced myocardial damage and its mecha-nisms. Methods 35 SD rats were randomly divided into five groups: control group, model group (epirubicin+saline); DEX1 group (epirubicin+low dose of dexrazoxane); DEX2 group (epirubicin+medium dose of dexrazoxane); DEX3 group (epirubicin+high dose of dexrazoxane). After administration, we detected the malondialdehyde (MDA) content and total superoxide dismutase (T-SOD) activity in myocardial tissues, plasma lactate dehydrogenase (LDH) levels of each group, and observed cardiomyocyte apoptosis in all groups. Results Compared with the control group, the SOD activity in myocardial tissue of model group was sig-nificantly decreased, and the MDA content in myocardial tissue, the plasma LDH content, and myocardial cell apoptotic index were significantly increased (P<0.01). Compared with the model group, the SOD activity in myocardial tissue of rats treated by different doses of dexrazoxane was markedly increased, and the MDA content in myocardial tissue, the plasma LDH content, and myocardial cell apoptotic index were significantly decreased (P<0.01 or P<0.05). Conclusion Dexrazoxane could relieve pharmorubicin-induced myocardial apoptosis. This may be associated with that it could reduce the produce of oxygen radical and lipid peroxidation.

关键词

右丙亚胺/蒽环类药物/心脏毒性/细胞凋亡

Key words

Dexrazoxane/Pharmorubicin/Cardiotoxicity/Apoptosis

分类

医药卫生

引用本文复制引用

吴晖,欧阳取长,刘莉萍,鲁军,水峥嵘..右丙亚胺对表柔比星致大鼠心肌损伤的保护作用及机制研究[J].肿瘤药学,2014,(1):40-45,6.

基金项目

湖南省卫生厅资助项目(B2012-094)。 ()

肿瘤药学

2095-1264

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