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Resveratrol attenuates doxorubicin-induced cardiomyocyte apoptosis in mice through SIRT1-mediated deacetylation of p53

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WOS被引频次:90
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成果类型:
期刊论文
作者:
Chi Zhang;Yansheng Feng;Shunlin Qu;Xing Wei;Honglin Zhu;Qi Luo;Meidong Liu;Guangwen Chen;Xianzhong Xiao;Chi Zhang;Yansheng Feng;Shunlin Qu;Xing Wei;Honglin Zhu;Qi Luo;Meidong Liu;Guangwen Chen;Xianzhong Xiao
通讯作者:
Xiao, XZ
作者机构:
[Shunlin Qu; Meidong Liu; Honglin Zhu; Chi Zhang; Guangwen Chen; Qi Luo; Yansheng Feng; Xianzhong Xiao; Xing Wei] Cent S Univ, Xiangya Sch Med, Dept Pathophysiol, Changsha 410078, Hunan, Peoples R China.
[Shunlin Qu; Chi Zhang; Xing Wei] Univ S China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, Hengyang 421001, Hunan, Peoples R China.
通讯机构:
[Xiao, XZ] Cent S Univ, Xiangya Sch Med, Dept Pathophysiol, 110 Xiangya Rd, Changsha 410078, Hunan, Peoples R China.
语种:
英文
关键词:
Resveratrol;Doxorubicin;SIRT1;p53;Apoptosis
期刊:
Cardiovascular Research
ISSN:
0008-6363
年:
2011
卷:
90
期:
3
页码:
538-545
文献类别:
WOS:Article
所属学科:
ESI学科类别:临床医学;WOS学科类别:Cardiac & Cardiovascular Systems
入藏号:
PMID:21278141
基金类别:
Major National Basic Research Program of China [2007CB512007]
机构署名:
本校为其他机构
院系归属:
医学院
摘要:
Aims Doxorubicin (DOX) is an anthracycline drug with a wide spectrum of clinical antineoplastic activity, but increased apoptosis has been implicated in its cardiotoxicity. Resveratrol (RES) was shown to harbour major health benefits in diseases associated with oxidative stress. In this study, we aimed to determine the effect of RES on DOX-induced myocardial apoptosis in mice.;Methods and results Male Balb/c mice were randomized to one of the following four treatments: saline, RES, DOX, or RES plus DOX (10 mice in each group). DOX treatment markedly depressed cardiac function, decreased the heart weight, the body weight, and the ratio of heart weight to body weight, but inversely increased the level of protein carbonyl, malondialdehyde, and serum lactate dehydrogenase, and induced mitochondrial cytochrome c release and cardiomyocyte apoptosis. However, these effects of DOX were ameliorated by its combination with RES. Further studies with a co-immunoprecipitation assay revealed an interaction between p53 and Sirtuin 1 (SIRT1). It was found by western blot and electrophoretic mobility shift assay that DOX treatment increased p53 protein acetylation and cytochrome c release from mitochondria, activated p53 binding at the Bax promoter, and up-regulated Bax expression, but supplementation with RES could weaken all these effects.;Conclusion The protective effect of RES against DOX-induced cardiomyocyte apoptosis is associated with the up-regulation of SIRT1-mediated p53 deacetylation.
参考文献:
Baur JA, 2006, NAT REV DRUG DISCOV, V5, P493, DOI 10.1038/nrd2060
Erster S, 2005, BIOCHEM BIOPH RES CO, V331, P843, DOI 10.1016/j.bbrc.2005.03.187
El-Mowafy AM, 1999, FEBS LETT, V451, P63, DOI 10.1016/S0014-5793(99)00541-4
Vaziri H, 2001, CELL, V107, P149, DOI 10.1016/S0092-8674(01)00527-X
Nakamura T, 2000, CIRCULATION, V102, P572

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