| Literature DB >> 30857673 |
Wencong Tian1, Lei Yang2, Yuansheng Liu3, Jianxiang He3, Liang Yang3, Qiong Zhang4, Fei Liu3, Jing Li3, Jie Liu3, Shoichiro Sumi5, Yanna Shen6, Zhi Qi7.
Abstract
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.Entities:
Keywords: Resveratrol Doxorubicin VEGF-B Cardiotoxicity Apoptosis
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Year: 2019 PMID： 30857673 DOI： 10.1016/j.jnutbio.2019.01.018
Source DB: PubMed Journal: J Nutr Biochem ISSN： 0955-2863 Impact factor: 6.048