title: [Effect and mechanism of intermedin in acute rat cardiac ischemic injury].
abstract: OBJECTIVE
  To investigate the effect and potential mechanism of intermedin (IMD) in acute cardiac ischemic injury and to provide a new approach for exploring mechanism of sudden cardiac death.
  
  
  METHODS
  Seventy-two healthy male rats were randomly divided into 3 groups: control, ischemic and the IMD-treated group. The activity of lactate dehydrogenase (LDH), malondialdehyde (MDA) and superoxide dismutase (SOD) in heart blood were tested by enzyme chemistry method. The mRNA changes of calcitonin receptor-like receptor (CRLR) and receptor activity-modifying proteins (RAMPs) in cardiac were measured by real-time PCR analysis. Myocardial cyclic adenosine monophosphate (cAMP) content was determined by enzyme linked immunosorbent assay (ELISA). Apoptosis related factors Bcl-2 and Bax were detected by immunohistochemistry.
  
  
  RESULTS
  Comparing with the control group, LDH and MDA activity of ischemic group in heart blood increased and SOD activity decreased. The concentration of cAMP increased in ventricular muscle, Bcl-2 and Bax proteins expression ratio level decreased. The intravenation of IMD decreased the level of increased activity of LDH and MDA, and lessened the level of decreased activity of SOD. The mRNA expression of CRLR and RAMPs obviously increased in ventricular muscle.
  
  
  CONCLUSIONS
  The protective effect of IMD against myocardial ischemic injury could be caused by decreasing the oxidative stress of ischemia and inhibiting the myocardial apoptosis.
authors: Department of Forensic Pathology, School of Forensic Medicine, Shanxi Medical University, Taiyuan 030001, China. dqx_2008@126.com
authors: Qiu-Xiang
authors: QX
authors: Du
authors: Wei
authors: W
authors: Yue
authors: Ying-Yuan
authors: YY
authors: Wang
mesh_terms: D053607:Adrenomedullin / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D058286:Calcitonin Receptor-Like Protein / Q000235:genetics / Q000378:metabolism; D002316:Cardiotonic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism; D004195:Disease Models, Animal; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D017202:Myocardial Ischemia / Q000378:metabolism / Q000473:pathology*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D009479:Neuropeptides / Q000008:administration & dosage / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D058261:Receptor Activity-Modifying Proteins / Q000235:genetics / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: C499411:Adm2 protein, rat; D058286:Calcitonin Receptor-Like Protein; D002316:Cardiotonic Agents; D009479:Neuropeptides; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D058261:Receptor Activity-Modifying Proteins; D053607:Adrenomedullin; D008315:Malondialdehyde; D000242:Cyclic AMP; D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase