Мақола

Resveratrol protects cardiomyocytes from doxorubicin-induced apoptosis through the AMPK/P53 pathway

Mi‐Hua LiuDepartment of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. ChinaXiao‐Long LinDepartment of Pathology, The Third People's Hospital of Huizhou Affiliated to Guangzhou Medical University, Huizhou, Guangdong 516002, P.R. ChinaDongming GuoLaboratory of Clinical Anatomy, University of South China, Hengyang, Hunan 421001, P.R. ChinaYuan ZhangDepartment of Pathology, Mawangdui Hospital, Changsha, Hunan 410016, P.R. ChinaCong YuanDepartment of Cardiology, The First Hospital of Changsha, Changsha, Hunan 410005, P.R. ChinaTIAN-PING TANDepartment of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. ChinaYu-Dan ChenDepartment of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. ChinaSHAO-JIAN WUDepartment of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. ChinaZufeng YeDepartment of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. ChinaJun HeDepartment of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China

2015en

ABI

Аннотация

Doxorubicin (DOX) is an efficient drug used in cancer therapy; however, it has severe cardiotoxic side effects. The aim of the present study was to investigate the effects of resveratrol on the adenosine monophosphate-activated protein kinase (AMPK)/P53 pathway in mediating DOX-induced cytotoxicity. H9c2 cells were exposed to 5 µM DOX for 24 h to establish a model of DOX-induced cardiotoxicity. DOX administration ampliﬁed P53 and B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax) expression and decreased Bcl-2 expression in H9c2 cells. Resveratrol increased the cell viability and decreased the apoptotic rate. In addition, resveratrol markedly increased the phosphorylation of AMPK. Of note, resveratrol protected against DOX-induced increases of P53 and Bax and also prevented the downregulation of Bcl-2 in H9c2 cells. Furthermore, AMPK inhibitor Compound C abolished the protective effects of resveratrol. The results of the present study therefore indicated that resveratrol protected H9c2 cells from DOX-induced apoptosis via the AMPK/P53 pathway.

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Идентификаторлар

DOI: 10.3892/mmr.2015.4665

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