title: Beneficial effects of growth hormone-releasing peptide on myocardial oxidative stress and left ventricular dysfunction in dilated cardiomyopathic hamsters.
abstract: BACKGROUND
  Growth hormone-releasing peptide (GHRP) may act directly on the myocardium and improve left ventricular (LV) function, suggesting a potential new approach to the treatment of cardiomyopathic hearts. The present study tested the hypothesis that the beneficial cardiac effects of GHRP might include attenuation of myocardial oxidative stress.
  
  
  RESULTS
  Dilated cardiomyopathic TO-2 hamsters were injected with GHRP-2 (1 mg/kg) or saline from 6 to 12 weeks of age. F1B hamsters served as controls. Untreated TO-2 hamsters progressively developed LV dilation, wall thinning, and systolic dysfunction between 6 and 12 weeks of age. Marked myocardial fibrosis was apparent in untreated hamsters at 12 weeks of age in comparison with F1B controls. The ratio of reduced to oxidized glutathione (GSH/GSSG) was decreased and the concentration of 4-hydroxynonenal (4-HNE) was increased in the hearts of untreated TO-2 hamsters. Treatment with GHRP-2 attenuated the progression of LV remodeling and dysfunction, as well as myocardial fibrosis, in TO-2 hamsters. GHRP-2 also inhibited both the decrease in the GSH/GSSG ratio and the increase in the concentration of 4-HNE in the hearts of TO-2 hamsters.
  
  
  CONCLUSIONS
  GHRP-2 can suppress the increase in the level of myocardial oxidative stress, leading to attenuation of progressive LV remodeling and dysfunction in dilated cardiomyopathic hamsters. (Circ J 2010; 74: 163 - 170).
authors: Pathophysiological Laboratory Sciences, Graduate School of Medicine, Nagoya University, Nagoya, Japan.
authors: Yosuke
authors: Y
authors: Kato
authors: Mitsunori
authors: M
authors: Iwase
authors: Sahoko
authors: S
authors: Ichihara
authors: Hiroaki
authors: H
authors: Kanazawa
authors: Katsunori
authors: K
authors: Hashimoto
authors: Akiko
authors: A
authors: Noda
authors: Kohzo
authors: K
authors: Nagata
authors: Yasuo
authors: Y
authors: Koike
authors: Mitsuhiro
authors: M
authors: Yokota
mesh_terms: D000447:Aldehydes / Q000378:metabolism; D000818:Animals; D002311:Cardiomyopathy, Dilated / Q000235:genetics / Q000378:metabolism*; D006224:Cricetinae; D004195:Disease Models, Animal; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D008297:Male; D008647:Mesocricetus; D009154:Mutation; D009206:Myocardium / Q000378:metabolism*; D009842:Oligopeptides / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects*; D049031:Sarcoglycans / Q000235:genetics; D013482:Superoxide Dismutase / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000378:metabolism*; D020257:Ventricular Remodeling / Q000187:drug effects / Q000502:physiology
chemical_list: D000447:Aldehydes; D009842:Oligopeptides; D049031:Sarcoglycans; C091874:growth hormone-releasing peptide-2; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione; C027576:4-hydroxy-2-nonenal; D019803:Glutathione Disulfide