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Rosiglitazone-induced myocardial protection against ischaemia-reperfusion injury is mediated via a phosphatidylinositol 3-kinase/Akt-dependent pathway
Zhang, Xue-Jiao1; Xiong, Zi-Bo2; Tang, An-Li1; Ma, Hong1; Ma, Yue-Dong1; Wu, Jing-Guo1; Dong, Yu-Gang1
关键词Akt ischaemia myocardial infarction peroxisome proliferator-activated receptor gamma phosphatidylinositol 3-kinase rosiglitazone
刊名CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
2010-02-01
DOI10.1111/j.1440-1681.2009.05232.x
37期:2页:156-161
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Pharmacology & Pharmacy ; Physiology
研究领域[WOS]Pharmacology & Pharmacy ; Physiology
关键词[WOS]ACTIVATED-RECEPTOR-GAMMA ; GLYCOGEN-SYNTHASE KINASE-3-BETA ; CARDIOMYOCYTES IN-VITRO ; K-ATP CHANNELS ; ISCHEMIA/REPERFUSION INJURY ; PPAR-GAMMA ; 3-KINASE PATHWAY ; CELL-SURVIVAL ; APOPTOSIS ; HEART
英文摘要

1. Rosiglitazone is widely used in the treatment of Type 2 diabetes. However, in recent years it has become evident that the therapeutic effects of peroxisome proliferator-activated receptor gamma ligands reach far beyond their use as insulin sensitizers. Recently, the ability of rosiglitazone pretreatment to induce cardioprotection following ischaemia-reperfusion (I/R) has been well documented; however, the protective mechanisms have not been elucidated. In the present study, examined the role of the phosphatidylinositol 3-kinase (PI3-K)/Akt signalling pathway in rosiglitazone cardioprotection following I/R injury.

2. Mice were pretreated with 3 mg/kg per day rosiglitazone for 14 days before hearts were subjected to ischaemia (30 min) and reperfusion (2 h). Wortmannin (1.4 mg/kg, i.p.), an inhibitor of PI3-K, was administered 10 min prior to myocardial I/R. Then, activation of the PI3-K/Akt/glycogen synthase kinase (GSK)-3 alpha signalling pathway was examined. The effects of PI3-K inhibition on rosiglitazone-induced cardioprotection were also evaluated.

3. Compared with control rats, the ratio of infarct size to ischaemic area (area at risk) and the occurrence of sustained ventricular fibrillation in rosiglitazone-pretreated rats was significantly reduced (P < 0.05). Rosiglitazone pretreatment attenuated cardiac apoptosis, as assessed by ELISA to determine cardiomyocyte DNA fragmentation. Rosiglitazone pretreatment significantly increased levels of phosphorylated (p-) Akt and p-GSK-3 alpha in the rat myocardium. Pharmacological inhibition of PI3-K by wortmannin markedly abolished the cardioprotection induced by rosiglitazone.

4. These results indicate that rosiglitazone-induced cardioprotection in I/R injury is mediated via a PI3-K/Akt/GSK-3 alpha-dependent pathway. The data also suggest that modulation of PI3-K/Akt/GSK-3 alpha-dependent signalling pathways may be a viable strategy to reduce myocardial I/R injury.

语种英语
WOS记录号WOS:000273821300015
引用统计
被引频次:16[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/64486
专题北京大学深圳医院_肾内科
作者单位1.Sun Yat Sen Univ, Affiliated Hosp 1, Dept Cardiol, Guangzhou 510080, Guangdong, Peoples R China
2.Peking Univ, Shenzhen Hosp, Div Renal, Shenzhen, Guangdong, Peoples R China
推荐引用方式
GB/T 7714
Zhang, Xue-Jiao,Xiong, Zi-Bo,Tang, An-Li,et al. Rosiglitazone-induced myocardial protection against ischaemia-reperfusion injury is mediated via a phosphatidylinositol 3-kinase/Akt-dependent pathway[J]. CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY,2010,37(2):156-161.
APA Zhang, Xue-Jiao.,Xiong, Zi-Bo.,Tang, An-Li.,Ma, Hong.,Ma, Yue-Dong.,...&Dong, Yu-Gang.(2010).Rosiglitazone-induced myocardial protection against ischaemia-reperfusion injury is mediated via a phosphatidylinositol 3-kinase/Akt-dependent pathway.CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY,37(2),156-161.
MLA Zhang, Xue-Jiao,et al."Rosiglitazone-induced myocardial protection against ischaemia-reperfusion injury is mediated via a phosphatidylinositol 3-kinase/Akt-dependent pathway".CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY 37.2(2010):156-161.
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