详情页 - 首都医科大学宣武医院知识库

当前位置：首页 > 详情页

Dexrazoxane ameliorates doxorubicin-induced cardiotoxicity by inhibiting both apoptosis and necroptosis in cardiomyocytes

文献详情

资源类型：

作者：

机构： [a]Peking University Fifth School of Clinical Medicine, Beijing, 100730, China [b]The Key Laboratory of Geriatrics, Beijing Institute of Geriatrics, Beijing Hospital, National Center of Gerontology, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, P.R. China, Beijing, 100730, China [c]Beijing Tiantan Hospital, Capital Medical University, Beijing, 100070, China

出处：

DOI：

ISSN：

关键词： Apoptosis Dexrazoxane Doxorubicin Necroptosis NF-κB p38MAPK

摘要：

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-κB pathways. These results indicated that dexrazoxane ameliorates cardiotoxicity and protects heart function by attenuating both apoptosis and necroptosis in doxorubicin induced cardiomyocyte injury. © 2019 Elsevier Inc.

基金：

语种：

中科院(CAS)分区：

出版当年[2018]版：

大类 | 3 区生物

小类 | 3 区生物物理 4 区生化与分子生物学

最新[2023]版：

大类 | 3 区生物学

小类 | 3 区生物物理 4 区生化与分子生物学

第一作者：

推荐引用方式(GB/T 7714)：

APA：

MLA：

相关文献

[1]SIRT1 Suppresses Doxorubicin-Induced Cardiotoxicity by Regulating the Oxidative Stress and p38MAPK Pathways [2]大鼠脑缺血再灌注损伤后NF-κB蛋白、Caspase3 mRNA表达及细胞凋亡的研究 [3]大鼠脑缺血再灌注损伤后NF-κB蛋白、Caspase3 mRNA表达及细胞凋亡的研究 [4]凋亡通路参与姜黄素抑制THP-1细胞炎症因子的转录（英文） [5]Polygalacic acid attenuates cognitive impairment by regulating inflammation through PPARγ/NF-κB signaling pathway [6]核因子-κB在哮喘患儿支气管上皮细胞的活化及意义 [7]N-乙酰半胱氨酸对大鼠急性坏死性胰腺炎胰腺损伤的影响 [8]脑静脉血栓形成的临床诊断及病因分析 [9]Increase of TNFα-stimulated Osteoarthritic Chondrocytes Apoptosis and Decrease of Matrix Metalloproteinases 9 by NF-κB Inhibition [10]促黑素细胞激素的抗炎机制