Intermedin protects against myocardial ischemia-reperfusion injury in diabetic rats

Cardiovascular Diabetology

Original Investigation

Hong Li¹  Cheng Wang¹  Yunfei Bian¹  Nana Zhang¹  Jia Guo¹  Chuanshi Xiao¹  Wayne Bond Lau² 

[1] Department of Cardiology, Shanxi Medical University, 030001, Taiyuan, Shanxi, China;Department of Emergency Medicine, Thomas Jefferson University, 19107, Philadelphia, PA, USA;

关键词: Intermedin;    Ischemia-reperfusion;    Diabetes;    Oxidative stress;    Apoptosis;    Inflammatory;   

DOI  :  10.1186/1475-2840-12-91

 received in 2013-04-17, accepted in 2013-06-14,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundDiabetic patients, through incompletely understood mechanisms, endure exacerbated ischemic heart injury compared to non-diabetic patients. Intermedin (IMD) is a novel calcitonin gene-related peptide (CGRP) superfamily member with established cardiovascular protective effects. However, whether IMD protects against diabetic myocardial ischemia/reperfusion (MI/R) injury is unknown.MethodsDiabetes was induced by streptozotocin in Sprague–Dawley rats. Animals were subjected to MI via left circumflex artery ligation for 30 minutes followed by 2 hours R. IMD was administered formally 10 minutes before R. Outcome measures included left ventricular function, oxidative stress, cellular death, infarct size, and inflammation.ResultsIMD levels were significantly decreased in diabetic rats compared to control animals. After MI/R, diabetic rats manifested elevated intermedin levels, both in plasma (64.95 ± 4.84 pmol/L, p < 0.05) and myocardial tissue (9.8 ± 0.60 pmol/L, p < 0.01) compared to pre-MI control values (43.62 ± 3.47 pmol/L and 4.4 ± 0.41). IMD administration to diabetic rats subjected to MI/R decreased oxidative stress product generation, apoptosis, infarct size, and inflammatory cytokine release (p < 0.05 or p < 0.01).ConclusionsBy reducing oxidative stress, inflammation, and apoptosis, IMD may represent a promising novel therapeutic target mitigating diabetic ischemic heart injury.

【 授权许可】

Unknown   
© Li et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.