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2275899 
Journal Article 
Intermedin protects against myocardial ischemia-reperfusion injury in diabetic rats 
Li, H; Bian, Y; Zhang, N; Guo, Jia; Wang, C; Lau, WB; Xiao, C 
2013 
Yes 
Cardiovascular Diabetology
ISSN: 1475-2840 
12 
23777472 
WOS:000321346000001 
Background: Diabetic 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. Methods: Diabetes 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. Results: IMD 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). Conclusions: By reducing oxidative stress, inflammation, and apoptosis, IMD may represent a promising novel therapeutic target mitigating diabetic ischemic heart injury. 
Intermedin; Ischemia-reperfusion; Diabetes; Oxidative stress; Apoptosis; Inflammatory