title: Intermedin protects against myocardial ischemia-reperfusion injury in diabetic rats.
abstract: 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.
authors.forename: Hong
authors.initials: H
authors.lastname: Li
authors.forename: Yunfei
authors.initials: Y
authors.lastname: Bian
authors.forename: Nana
authors.initials: N
authors.lastname: Zhang
authors.forename: Jia
authors.initials: J
authors.lastname: Guo
authors.forename: Cheng
authors.initials: C
authors.lastname: Wang
authors.forename: Wayne Bond
authors.initials: WB
authors.lastname: Lau
authors.forename: Chuanshi
authors.initials: C
authors.lastname: Xiao
mesh_terms: D053607:Adrenomedullin / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002316:Cardiotonic Agents / Q000494:pharmacology*; D016207:Cytokines / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D058065:Diabetic Cardiomyopathies / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D009479:Neuropeptides / Q000378:metabolism / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects; D017207:Rats, Sprague-Dawley; D013311:Streptozocin; D013997:Time Factors; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: C499411:Adm2 protein, rat; D002316:Cardiotonic Agents; D016207:Cytokines; D018836:Inflammation Mediators; D009479:Neuropeptides; D053607:Adrenomedullin; D013311:Streptozocin