重组白细胞介素-1对仓鼠阿霉素诱导的心脏毒性的预防作用。阿霉素心脏毒性与白细胞介素-1

Prevention of doxorubicin-induced cardiotoxicity by recombinant interleukin-1 in hamsters. Doxorubicin cardiotoxicity and interleukin-1.

作者信息

Yoshida T, Okumura H, Kaya H, Okabe Y, Matano S, Ohtake S, Nakamura S, Matsuda T

机构信息

Department of Internal Medicine, Toyama Perefectural Central Hospital, Japan.

出版信息

Biotherapy. 1993;6(2):125-32. doi: 10.1007/BF01877425.

DOI:10.1007/BF01877425

PMID:8398571

Abstract

The major factor contributing to doxorubicin (DXR)-induced cardiotoxicity is the insufficiency of antioxidant defense mechanisms. As a model of acute cardiotoxicity with DXR, ten-week-old golden hamsters were given DXR (5 mg/kg) intravenously, and the toxicity was investigated by monitoring ECG changes. Complete A-V block and cardiac arrest on the ECG were observed in DXR-treated hamsters. DXR-induced edema and fragmentation of myofibrils were observed by electron-micrograph. Pretreatment with interleukin-1 beta (10 or 1 microgram/body) 12 or 24 hrs before prevented these changes, but pretreatment with tumor necrosis factor alpha had no effect.

摘要

导致阿霉素（DXR）诱导的心脏毒性的主要因素是抗氧化防御机制不足。作为DXR急性心脏毒性的模型，给10周龄的金黄仓鼠静脉注射DXR（5毫克/千克），并通过监测心电图变化来研究毒性。在接受DXR治疗的仓鼠中观察到心电图上出现完全性房室传导阻滞和心脏骤停。通过电子显微镜观察到DXR诱导的肌原纤维水肿和断裂。在注射前12或24小时用白细胞介素-1β（10或1微克/只）预处理可预防这些变化，但用肿瘤坏死因子α预处理则无效。