Resveratrol inhibits doxorubicin‑induced cardiotoxicity via sirtuin 1 activation in H9c2 cardiomyocytes

Liu,Mi‑Hua; Shan,Jian; Li,Jian; Zhang,Yuan; Lin,Xiao‑Long

doi:10.3892/etm.2016.3437

Resveratrol inhibits doxorubicin‑induced cardiotoxicity via sirtuin 1 activation in H9c2 cardiomyocytes

Authors:
- Mi‑Hua Liu
- Jian Shan
- Jian Li
- Yuan Zhang
- Xiao‑Long Lin
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Affiliations: Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China, Department of Pathology, Zhongshan Torch Development Zone Hospital, Zhongshan, Guangdong 528437, P.R. China, Department of Ultrasonic Diagnosis, Bo'Ai Hospital of Zhongshan, Zhongshan, Guangdong 528403, P.R. China, Department of Pathology, Mawangdui Hospital, Changsha, Hunan 410016, P.R. China, Department of Pathology, The Third People's Hospital of Huizhou, Affiliated Huizhou Hospital of Guangzhou Medical University, Huizhou, Guangdong 516002, P.R. China
Published online on: June 8, 2016 https://doi.org/10.3892/etm.2016.3437
Pages: 1113-1118

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Abstract

Doxorubicin (DOX) is an efficient drug used in cancer therapy; however, it can induce severe cytotoxicity, which limits its clinical application. In the present study, the effects of resveratrol (RES) on sirtuin 1 (SIRT1) activation in mediating DOX‑induced cytotoxicity in H9c2 cardiac cells was investigated. H9c2 cells were exposed to 5 µM DOX for 24 h to establish a model of DOX cardiotoxicity. Apoptosis of H9c2 cardiomyocytes was assessed using the MTT assay and Hoechst nuclear staining. The results demonstrated that pretreating H9c2 cells with RES prior to the exposure of DOX resulted in increased cell viability and a decreased quantity of apoptotic cells. Western blot analysis demonstrated that DOX decreased the expression level of SIRT1. These effects were significantly alleviated by co‑treatment with RES. In addition, the results demonstrated that DOX administration amplified forkhead box O1 (FoxO1) and P53 expression levels in H9c2 cells. RES was also found to protect against DOX‑induced increases of FoxO1 and P53 expression levels in H9c2 cells. Furthermore, the protective effects of RES were arrested by the SIRT1 inhibitor nicotinamide. In conclusion, the results demonstrated that RES protected H9c2 cells against DOX‑induced injuries via SIRT1 activation.

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