期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 523, 期 1, 页码 140-146出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2019.12.027
关键词
Dexrazoxane; Doxorubicin; Necroptosis; Apoptosis; p38MAPK; NF-kappa B
资金
- National Natural Science Foundation of China [81770228, 81470427, 31400995, 81770858]
- Beijing Natural Science Foundation [7142142, 7154234]
- Beijing Hospital Nova project [BJ-2016-045, BJ-2016-034, BJ-2018-138, BJ-2016-032]
- NonProfit Central Research Institute Fund of the Chinese Academy of Medical Sciences [2018RC310025]
- Special Subsidy Project of Beijing Municipal Science and Technology Commission on the Application Research of Capital Clinical Characteristics [Z181100001718138]
Doxorubicin, as a first line chemotherapeutic agent, its usage is limited owing to cardiotoxicity. Necroptosis is a new form of programmed cell death, and recent investigations indicated that necroptosis is vitally involved in serious cardiac pathological conditions. Dexrazoxane is the only cardiac protective drug approved by FDA for anthracycline. We aimed to explore whether and how dexrazoxane regulates doxorubicin-induced cardiomyocyte necroptosis. First, doxorubicin could cause heart failure and reduce cardiomyocyte viability by promoting cell apoptosis and necroptosis in vivo and in vitro. Second, necroptosis plays an important role in doxorubicin induced cardiomyocyte injury, which could be inhibited by Nec-1. Third, dexrazoxane increased cell viability and protect heart function by decreasing both cardiomyocyte apoptosis and necroptosis after doxorubicin treatment. Forth, dexrazoxane attenuated doxorubicin-induced inflammation and necroptosis by the inhibition of p38MAPK/NF-kappa B pathways. These results indicated that dexrazoxane ameliorates cardiotoxicity and protects heart function by attenuating both apoptosis and necroptosis in doxorubicin induced cardiomyocyte injury. (C) 2019 Elsevier Inc. All rights reserved.
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