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学科主题: 临床医学
题名:
Inhibition of endoplasm reticulum stress by ghrelin protects against ischemia/reperfusion injury in rat heart
作者: Zhang, Gai-Gai1; Teng, Xu2; Liu, Yue1; Cai, Yan2; Zhou, Ye-Bo2; Duan, Xiao-Hui2; Song, Jun-Qiu2; Shi, Yi2; Tang, Chao-Shu2,3,4; Yin, Xin-Hua1; Qi, Yong-Fen2,3,4
关键词: Ghrelin ; Ischemia/reperfusion injury ; Endoplasmic reticulum stress ; Apoptosis ; Unfolded protein response
刊名: PEPTIDES
发表日期: 2009-06-01
DOI: 10.1016/j.peptides.2009.03.024
卷: 30, 期:6, 页:1109-1116
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]: ENDOTHELIAL-CELLS ; IN-VITRO ; MYOCARDIAL-INFARCTION ; OXIDATIVE STRESS ; ISCHEMIC-INJURY ; PREVENTS ; KINASE ; DEATH ; CARDIOMYOCYTES ; ATTENUATION
英文摘要:

Ghrelin is a multi-functional polypeptide with cardiovascular protective effects. We aimed to explore whether the cardioprotective effect of ghrelin is mediated by inhibiting myocardial endoplasmic reticulum stress (ERS). A Langendorff model of isolated rat heart was used with ischemia/reperfusion (I/R; 40/120 min). Cardiac function was monitored, and histomorphologic features, degree of myocardial injury, level of ERS markers, and number of apoptotic cardiomyocytes were determined. Compared with control group, the I/R group showed significantly decreased cardiac function, seriously damaged myocardial tissue, increased number of apoptotic cells, and overexpression of mRNA and protein of ERS markers. However, preadministration of ghrelin in vivo (10(-8) mol/kg, intraperitoneal injection, every 12 h, twice in all) greatly ameliorated the damaged heart function, attenuated myocardial injury and apoptosis, and decreased the expression of ERS markers: it decreased the mRNA and protein levels of glucose-regulated protein78 (GRP78) and C/EBP homologous protein (CHOP), with reduced caspase-12 protein expression. Furthermore, in vitro, ghrelin directly inhibited the myocardial ERS response induced by tunicamycin or dithiothreitol in rat cardiac tissue. Ghrelin could protect the heart against I/R injury, at least in part, through inhibiting myocardial ERS. (C) 2009 Published by Elsevier Inc.

语种: 英语
所属项目编号: 30670847 ; 2006CB503807
项目资助者: National Natural Science Foundation of China ; State Major Basic Research Development Program of the People&prime ; s Republic of China
WOS记录号: WOS:000267006700013
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/50535
Appears in Collections:北京大学第一临床医学院_心血管内科_期刊论文

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作者单位: 1.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China
2.Harbin Med Coll, Affiliated Hosp 2, Dept Cardiol, Harbin 150086, Peoples R China
3.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China
4.Peking Univ, Hosp 1, Inst Cardiovasc Dis, Beijing 100034, Peoples R China

Recommended Citation:
Zhang, Gai-Gai,Teng, Xu,Liu, Yue,et al. Inhibition of endoplasm reticulum stress by ghrelin protects against ischemia/reperfusion injury in rat heart[J]. PEPTIDES,2009,30(6):1109-1116.
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