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学科主题: 基础医学
题名:
ROCK-dependent ATP5D modulation contributes to the protection of notoginsenoside NR1 against ischemia-reperfusion-induced myocardial injury
作者: He, Ke1,2,3,4; Yan, Li2,3,4; Pan, Chun-Shui2,3,4; Liu, Yu-Ying2,3,4; Cui, Yuan-Chen1,2,3,4; Hu, Bai-He2,3,4; Chang, Xin2,3,4; Li, Quan2,3,4; Sun, Kai2,3,4; Mao, Xiao-Wei1,2,3,4; Fan, Jing-Yu2; Han, Jing-Yan1,2,3,4
关键词: notoginsenoside R1 ; myocardium ischemia-reperfusion injury ; apoptosis ; Rho kinase ; inhibition ; energy deficit
刊名: AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
发表日期: 2014-12-15
DOI: 10.1152/ajpheart.00259.2014
卷: 307, 期:12, 页:H1764-H1776
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cardiac & Cardiovascular Systems ; Physiology ; Peripheral Vascular Disease
研究领域[WOS]: Cardiovascular System & Cardiology ; Physiology
关键词[WOS]: ISCHEMIA/REPERFUSION INJURY ; PANAX-NOTOGINSENG ; KINASE INHIBITOR ; DELTA-SUBUNIT ; HEART ; SYNTHASE ; RATS ; R1 ; ACTIVATION ; FASUDIL
英文摘要:

Cardiac ischemia-reperfusion (I/R) injury remains a challenge for clinicians, which initiates with energy metabolism disorder. The present study was designed to investigate the protective effect of notoginsenoside R1 (NR1) on I/R-induced cardiac injury and underlying mechanism. Male Sprague-Dawley rats were subjected to 30-min occlusion of the left coronary anterior descending artery followed by reperfusion with or without NR1 pretreatment (5 mg.kg(-1).h(-1)). In vitro, H9c2 cells were cultured under oxygen and glucose deprivation/reoxygenation conditions after NR1 (0.1 mM), Rho kinase (ROCK) inhibitor Y-27632 (10 mu M), or RhoA/ROCK activator U-46619 (10 nM) administration. Myocardial infarct size, myocardial histology, and cardiac function were evaluated. Myofibril and mitochondria morphology were observed by transmission electron microscopy. F-actin and apoptosis were determined by immunofluorescence and TUNEL staining. ATP and AMP content were assessed by ELISA. Phosphorylated-AMP-activated protein kinase, ATP synthase subunits, apoptosis-related molecules, and the level and activity of ROCK were determined by Western blot analysis. We found that NR1 pretreatment ameliorated myocardial infarction, histological injury, and cardiac function induced by I/R. Furthermore, similar to the effect of Y-27632, NR1 improved H9c2 cell viability, maintained actin skeleton and mitochondria morphology, and attenuated apoptosis induced by oxygen and glucose deprivation/reoxygenation. Importantly, NR1 prevented energy abnormity, inhibited the expression and activation of ROCK, and restored the expression of the mitochondrial ATP synthase delta-subunit both in vivo and in vitro, whereas U-46619 suppressed the effect of NR1. These results prove NR1 as an agent able to prevent I/R-induced energy metabolism disorder via inhibiting ROCK and enhancing mitochondrial ATP synthase delta-subunits, which at least partially contributes to its protection against cardiac I/R injury.

语种: 英语
所属项目编号: 2013ZX09402202 ; 81273637
项目资助者: Production of New Medicine Program of Ministry of Science and Technology of China ; National Natural Science Foundation of China
WOS记录号: WOS:000346478200009
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内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/63081
Appears in Collections:基础医学院_期刊论文

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作者单位: 1.Peking Univ, Sch Basic Med Sci, Dept Integrat Chinese & Western Med, Beijing 100191, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Tasly Microcirculat Res Ctr, Beijing 100191, Peoples R China
3.State Adm Tradit Chinese Med Peoples Republ China, Key Lab Microcirculat, Beijing, Peoples R China
4.State Adm Tradit Chinese Med Peoples Republ China, Key Lab Stasis & Phlegm, Beijing, Peoples R China

Recommended Citation:
He, Ke,Yan, Li,Pan, Chun-Shui,et al. ROCK-dependent ATP5D modulation contributes to the protection of notoginsenoside NR1 against ischemia-reperfusion-induced myocardial injury[J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY,2014,307(12):H1764-H1776.
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