Beneficial Effects of Growth Hormone-Releasing Peptide on Myocardial Oxidative Stress and Left Ventricular Dysfunction in Dilated Cardiomyopathic Hamsters

• Kato Yosuke

  Pathophysiological Laboratory Sciences, Graduate School of Medicine, Nagoya University Department of Pathobiological Science and Technology, Faculty of Medicine, Tottori University

• Iwase Mitsunori

  Pathophysiological Laboratory Sciences, Graduate School of Medicine, Nagoya University Division of Integrated Medicine, Toyota Memorial Hospital

• Ichihara Sahoko

  Department of Human Functional Genomics, Life Science Research Center, Mie University

• Kanazawa Hiroaki

  School of Nursing, University of Shizuoka

• Hashimoto Katsunori

  Pathophysiological Laboratory Sciences, Graduate School of Medicine, Nagoya University

• Noda Akiko

  Pathophysiological Laboratory Sciences, Graduate School of Medicine, Nagoya University

• Nagata Kohzo

  Pathophysiological Laboratory Sciences, Graduate School of Medicine, Nagoya University

• Koike Yasuo

  Pathophysiological Laboratory Sciences, Graduate School of Medicine, Nagoya University

• Yokota Mitsuhiro

  Department of Genome Science, School of Dentistry, Aichi-Gakuin University

抄録

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. Methods and 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)<br>

収録刊行物

• Circulation Journal

  Circulation Journal 74 (1), 163-170, 2010

  一般社団法人 日本循環器学会

キーワード

• Dilated cardiomyopathy
• Growth hormone-releasing peptide
• Hamsters
• Heart failure
• Oxidative stress

詳細情報

• CRID: 1390282680080582656
• NII論文ID: 10025941641
• NII書誌ID: AA11591968
• DOI: 10.1253/circj.cj-09-0378
• ISSN: 13474820
• ISSN: 13469843
• Web Site: http://www.jstage.jst.go.jp/article/circj/74/1/74_CJ-09-0378/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2010139076
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • CiNii Articles
  • KAKEN
• 抄録ライセンスフラグ: 使用不可