北京大学医学部机构知识库
Advanced  
IR@PKUHSC  > 基础医学院  > 期刊论文
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
Citation statistics:
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

Files in This Item:

There are no files associated with this item.


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.
Service
Recommend this item
Sava as my favorate item
Show this item's statistics
Export Endnote File
Google Scholar
Similar articles in Google Scholar
[He, Ke]'s Articles
[Yan, Li]'s Articles
[Pan, Chun-Shui]'s Articles
CSDL cross search
Similar articles in CSDL Cross Search
[He, Ke]‘s Articles
[Yan, Li]‘s Articles
[Pan, Chun-Shui]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Copyright © 2007-2017  北京大学医学部 - Feedback
Powered by CSpace