阿霉素心脏毒性发生机制及其防治的研究进展  

Researches on the mechanism of cardiomyocyte death from doxorubicin-induced cardiotoxicity and the control methods

作　　者：朱梁[1] 裴茂炜[2] 沈栋[2] 刘小玲[1] 

机构地区：[1]杭州师范大学医学实验中心,浙江杭州310036 [2]杭州师范大学临床医学院,浙江杭州310036

出　　处：《健康研究》2013年第2期102-105,共4页Health Research

基　　金：浙江省医药卫生科研计划基金项目(2012KYA169)

摘　　要：文章根据国内外最新研究进展,对阿霉素心脏毒性的临床表现、发生机制及预防措施作了综述。阿霉素是一种已被广泛使用的抗肿瘤药物,但因具有心脏毒性而使其使用受到限制。近年来的研究显示这种心脏毒性是通过心肌细胞凋亡和坏死这两种途径来实现的,而胞内活性氧自由基的积累和氧化应激系统的活化则是启动这一过程的最初原因。这个理论将有助于人们开发早期、敏感、特异的评估心脏毒性的监测方法,以及高效的针对DOX的心脏保护剂。This paper presents a review of the latest researches on the mechanism of cardiomyocyte death of doxorubicininduced cardiotoxicity and the control methods, focusing on the clinical characteristics, mechanism, clinical detection and the preventive measures. Adramycin is one of the most widely used and successful antitumor drugs. However, its cumulative and dose-dependent cardiac toxicity has been a major concern of cancer therapeutic practice for decades. Recently, many studies support the idea that eardiomyocyte death by apoptosis and necrosis is a primary mechanism of DOX-induced eardiomyopathy. It can be very helpful in protecting the heart by developing not only early-stage assessment of eardiotoxicity, which is sensitive and specific, but also highly effective DOX antagonists.

关 键 词：心肌细胞 阿霉素 心脏毒性 活性氧自由基 凋亡抑制剂 

分 类 号：R966[医药卫生—药理学]