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Cardioprotection by ischemic postconditioning is lost in isolated perfused heart from diabetic rats: Involvement of transient receptor potential vanilloid 1, calcitonin gene-related peptide and substance P
Ren, Jing-Yi; Song, Jun-Xian; Lu, Ming-Yu; Chen, Hong
关键词Ischemia/reperfusion Ischemic postconditioning Diabetes Transient receptor potential vanilloid 1 Calcitonin gene-related peptide Substance P
刊名REGULATORY PEPTIDES
2011-08-08
DOI10.1016/j.regpep.2011.04.004
169期:1-3页:49-57
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Endocrinology & Metabolism ; Physiology
研究领域[WOS]Endocrinology & Metabolism ; Physiology
关键词[WOS]REPERFUSION INJURY ; ACTIVATION ; CHANNELS ; TRPV1 ; ADRENOMEDULLIN ; EXPRESSION ; PROTECTS ; REFLEX ; NERVES ; MICE
英文摘要

We previously found that the expression of transient receptor potential vanilloid 1 (TRPV1) and contents of calcitonin gene-related peptide (CGRP) and substance P (SP), two main neuropeptides released from TRPV1, were decreased in diabetic hearts. This study aimed to test whether decreased TRPV1. CGRP and SP levels were responsible for the loss of cardioprotection by ischemic postconditioning (IPostC) in isolated perfused heart from streptozotocin-induced diabetic rats. IPostC effectively protected non-diabetic hearts against ischemia/reperfusion injury by improving cardiac function and lowering creatine kinase (CK) and cardiac troponin I (cTnI) release, which could be abolished by inhibiting TRPV1, CGRP receptor or SP receptor. However, IPostC had no effect on cardiac function and the release of CK and cTnI in diabetic hearts regardless of whether TRPV1, CGRP receptor or SP receptor were inhibited. CGRP or SP-induced postconditioning significantly prevented both non-diabetic and diabetic hearts from ischemia/reperfusion injury by improving cardiac function and lowering CK and cTnI release. Additionally. IPostC markedly increased CGRP and SP release in non-diabetic hearts, which could be reversed with TRPV1 inhibition, but not CGRP receptor or SP receptor inhibition. However, IPostC failed to affect CGRP and SP release in diabetic hearts in the presence or absence of TRPV1, CGRP receptor or SP receptor inhibition. These results indicate that the loss of cardioprotection by IPostC during diabetes is partly associated with a failure to increase CGRP and SP release, likely due to decreased TRPV1 expression and CGRP and SP contents in diabetic hearts. (C) 2011 Elsevier B.V. All rights reserved.

语种英语
WOS记录号WOS:000292368900008
项目编号7102157
资助机构Beijing Natural Science Foundation
引用统计
被引频次:35[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/400002259/60394
专题北京大学第二临床医学院_心血管内科
作者单位Peking Univ, Dept Cardiol, Peoples Hosp, Beijing 100044, Peoples R China
推荐引用方式
GB/T 7714
Ren, Jing-Yi,Song, Jun-Xian,Lu, Ming-Yu,et al. Cardioprotection by ischemic postconditioning is lost in isolated perfused heart from diabetic rats: Involvement of transient receptor potential vanilloid 1, calcitonin gene-related peptide and substance P[J]. REGULATORY PEPTIDES,2011,169(1-3):49-57.
APA Ren, Jing-Yi,Song, Jun-Xian,Lu, Ming-Yu,&Chen, Hong.(2011).Cardioprotection by ischemic postconditioning is lost in isolated perfused heart from diabetic rats: Involvement of transient receptor potential vanilloid 1, calcitonin gene-related peptide and substance P.REGULATORY PEPTIDES,169(1-3),49-57.
MLA Ren, Jing-Yi,et al."Cardioprotection by ischemic postconditioning is lost in isolated perfused heart from diabetic rats: Involvement of transient receptor potential vanilloid 1, calcitonin gene-related peptide and substance P".REGULATORY PEPTIDES 169.1-3(2011):49-57.
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