心脏毒性
阿霉素
药理学
乳酸脱氢酶
白藜芦醇
细胞凋亡
血管内皮生长因子
医学
体内
肌酸激酶
毒性
化疗
化学
生物
内分泌学
内科学
血管内皮生长因子受体
酶
生物化学
生物技术
作者
Wencong Tian,Lei Yang,Yuansheng Liu,Jianxiang He,Liang Yang,Qiong Zhang,Fei Liu,Jing Li,Jie Liu,Shoichiro Sumi,Yanna Shen,Zhi Qi
标识
DOI:10.1016/j.jnutbio.2019.01.018
摘要
Doxorubicin (DOX) is a broad spectrum antitumor agent. However, its clinical utility is limited due to the well-known cardiotoxicity. Resveratrol (RSV) has been reported to exert cardioprotective effect in some cardiovascular diseases. In this study, we aimed to determine the effect of RSV on DOX-induced cardiotoxicity, and further explore the underlying mechanism in this process.Male Sprague-Dawley (SD) rats were randomly divided into four groups: CON, DOX, RSV, or DOX+RSV group (10 rats in each group). DOX treatment significantly decreased cardiac function, and increased the release of serum lactate dehydrogenase (LDH) and creatine kinase isoenzyme (CK-MB) in rat serum. Increased cell death and apoptosis of cardiomyocytes were also observed in DOX group in comparison with CON group. DOX treatment dramatically down-regulated expression of VEGF-B either in vivo or in vitro. In contrast, the combination of RSV and DOX markedly attenuated DOX-induced cardiotoxicity with the up-regulation of VEGF-B. Inhibition of VEGF-B by small interfering RNA (siRNA) abolished the protective effects of RSV on DOX-treated cardiomyocytes.Consequently,our findings indicated that RSV attenuates DOX-induced cardiotoxicity through up-regulation of VEGF-B.
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