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学科主题基础医学
Extracellular signal-regulated kinase 1/2 activation is involved in intermedin1-53 attenuating myocardial oxidative stress injury induced by ischemia/reperfusion
Zhao, Lei2; Peng, Ding-Qiong3; Zhang, Jing4; Song, Jun-Qiu2; Teng, Xu2; Yu, Yan-Rong2; Tang, Chao-Shu1,2; Qi, Yong-Fen1
关键词Intermedin(1-53) Ischemia/reperfusion Oxidative Stress Myocardial Injury
刊名PEPTIDES
2012-02-01
DOI10.1016/j.peptides.2011.12.016
33期:2页:329-335
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Pharmacology & Pharmacy
研究领域[WOS]Biochemistry & Molecular Biology ; Pharmacology & Pharmacy
关键词[WOS]MICROVASCULAR ENDOTHELIAL-CELLS ; ISCHEMIA-REPERFUSION INJURY ; ISOLATED RAT HEARTS ; NAD(P)H OXIDASE ; IN-VITRO ; APOPTOSIS ; PATHWAY ; CARDIOPROTECTION ; CARDIOMYOCYTES ; HYPOXIA
英文摘要

Intermedin (IMD)(1-53) is a novel member of the calcitonin gene-related peptide superfamily and has potent cardioprotective effects against myocardial injury induced by ischemia-reperfusion (I/R). To explore the mechanism of the IMD1-53 cardioprotective effect, we studied the anti-oxidant effects of IMD1-53 on myocardial injury induced by I/R in vivo in rat and H2O2 treatment in vitro in rat cardiomyocytes. Compared with sham treatment, I/R treatment induced severe lipid peroxidation injury in rat myocardium: plasma malondialdehyde (MDA) content and myocardial LDH activity was increased by 34% and 85% (all P < 0.01); Mn-superoxide dismutase (Mn-SOD) and catalase (CAT) activity was reduced 80% and 86% (all P < 0.01), respectively, and the protein levels of the NADPH oxidase complex subunits gp91(phox) and p47(phox) were markedly increased, by 86% (P < 0.05) and 95% (P < 0.01), respectively; IMD1-53 treatment ameliorated lipid peroxidation injury: plasma MDA content and myocardial LDH activity was decreased by 30% (P < 0.05) and 36% (P < 0.01); Mn-SOD and CAT activity was elevated 1.0- and 4.3-fold (all P < 0.01), respectively; and the protein levels of gp91(phox) and p47(phox) were reduced, by 28% and 36% (both P < 0.05), respectively. Concurrently, IMD1-53 treatment markedly promoted cell viability and inhibited apoptosis in cardiomyocytes as compared with H2O2 treatment alone. Furthermore, IMD1-53 increased the ratio of p-ERK to ERK by 66% (P < 0.05) as compared with I/R alone, and the protective effect of IMD1-53 on H2O2-induced apoptosis was abolished by preincubation with PD98059. a MEK inhibitor. IMD1-53 may improve the oxidative stress injury induced by I/R via inhibiting the production of reactive oxygen species and enhancing ERK phosphorylation. (C) 2012 Elsevier Inc. All rights reserved.

语种英语
WOS记录号WOS:000301871200019
项目编号81170082 ; 30470693 ; 30770869
资助机构National Natural Science Foundation of China ; Beijing Education Bureau
引用统计
被引频次:33[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/400002259/51909
专题北京大学第二临床医学院_检验科
北京大学基础医学院
作者单位1.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China
2.Peking Univ, Sch Basic Med Sci, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China
3.Gen Hosp Civil Aviat Adm China, Dept Endocrinol, Beijing 100123, Peoples R China
4.Beijing Normal Univ, Sch PE & Sports Sci, Beijing 100875, Peoples R China
推荐引用方式
GB/T 7714
Zhao, Lei,Peng, Ding-Qiong,Zhang, Jing,et al. Extracellular signal-regulated kinase 1/2 activation is involved in intermedin1-53 attenuating myocardial oxidative stress injury induced by ischemia/reperfusion[J]. PEPTIDES,2012,33(2):329-335.
APA Zhao, Lei.,Peng, Ding-Qiong.,Zhang, Jing.,Song, Jun-Qiu.,Teng, Xu.,...&Qi, Yong-Fen.(2012).Extracellular signal-regulated kinase 1/2 activation is involved in intermedin1-53 attenuating myocardial oxidative stress injury induced by ischemia/reperfusion.PEPTIDES,33(2),329-335.
MLA Zhao, Lei,et al."Extracellular signal-regulated kinase 1/2 activation is involved in intermedin1-53 attenuating myocardial oxidative stress injury induced by ischemia/reperfusion".PEPTIDES 33.2(2012):329-335.
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