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学科主题: 基础医学
题名:
Extracellular signal-regulated kinase 1/2 activation is involved in intermedin1-53 attenuating myocardial oxidative stress injury induced by ischemia/reperfusion
作者: 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
发表日期: 2012-02-01
DOI: 10.1016/j.peptides.2011.12.016
卷: 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
所属项目编号: 81170082 ; 30470693 ; 30770869
项目资助者: National Natural Science Foundation of China ; Beijing Education Bureau
WOS记录号: WOS:000301871200019
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内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/51909
Appears in Collections:基础医学院_期刊论文

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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

Recommended Citation:
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.
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