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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Amelioration of doxorubicin-induced cardiotoxicity by deferiprone in rats.
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Amelioration of doxorubicin-induced cardiotoxicity by deferiprone in rats.

机译：去铁酮可改善阿霉素诱导的心脏毒性。

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摘要

The therapeutic usefulness of doxorubicin (Dox), an anthracycline antibiotic used as an anticancer agent, is limited by its cardiotoxicity. Dox-induced cardiotoxicity is mainly attributed to accumulation of reactive oxygen species and interaction of Dox with cellular iron metabolism. The present study investigated the effects of the iron chelator deferiprone (Def) against Dox-induced cardiotoxicity in rats. Dox (15 mg/kg) was injected intraperitoneally as a single dose, and Def (10 mg/kg) was administered orally for 10 days. Dox showed cardiotoxicity as evidenced by increased heart rate, elevated ST segment, prolonged QTc interval, and increased T wave amplitude. In addition, Dox enhanced aconitine cardiotoxicity by decreasing its dose, producing ventricular tachycardia. Administration of Def significantly attenuated Dox-induced electrocardiographic changes. Cardiotoxicity of Dox was confirmed biochemically by a significant elevation in serum creatine kinase-MB and lactate dehydrogenase activities as well as by myocardial malondialdehyde and reduced glutathione contents. Moreover, Dox caused a significant decrease in myocardial superoxide dismutase activity. Administration of Def significantly attenuated the biochemical changes. These results suggest that Def might be a potential cardioprotective agent against Dox-induced cardiotoxicity.
机译：阿霉素（一种用作抗癌药的蒽环类抗生素）的治疗作用受到其心脏毒性的限制。 Dox引起的心脏毒性主要归因于活性氧的积累以及Dox与细胞铁代谢的相互作用。本研究调查了铁螯合剂去铁酮（Def）对Dox诱导的大鼠心脏毒性的影响。腹膜内注射Dox（15 mg / kg）作为单剂，Def（10 mg / kg）口服10天。 Dox表现出心脏毒性，这由心率增加，ST段升高，QTc间隔延长和T波振幅增加所证明。此外，Dox通过降低其剂量增加乌头碱的心脏毒性，从而产生室性心动过速。 Def的给药显着减弱了Dox引起的心电图变化。 Dox的心脏毒性通过血清肌酸激酶-MB和乳酸脱氢酶活性的显着升高以及心肌丙二醛和谷胱甘肽含量的降低在生物化学上得到证实。而且，Dox引起心肌超氧化物歧化酶活性的显着降低。 Def的给药显着减弱了生化变化。这些结果表明，Def可能是对抗Dox诱导的心脏毒性的潜在心脏保护剂。

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