Effects of HMGB1 on Ischemia-Reperfusion Injury in the Rat Heart

• Oozawa Susumu

  Department of Cardiovascular Surgery, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

• Mori Shuji

  School of Pharmacy, University of Shujitsu

• Kanke Toru

  Department of Pharmacology, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

• Takahashi Hideo

  Department of Pharmacology, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

• Liu Keyue

  Department of Pharmacology, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

• Tomono Yasuko

  Shigei Medical Institute

• Asanuma Masato

  Department of Brain Science, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

• Miyazaki Ikuko

  Department of Brain Science, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

• Nishibori Masahiro

  Department of Pharmacology, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

• Sano Shunji

  Department of Cardiovascular Surgery, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences

抄録

Background Coronary ischemia-reperfusion (I/R) injury causes cardiomyocyte necrosis in a multi-step process that includes an inflammatory reaction. A recent study has suggested that high-mobility group box 1 (HMGB1) is a late mediator of lethal sepsis and an early mediator of inflammation and necrosis following I/R injury. In the present study a neutralizing monoclonal antibody (mAb) for HMGB1 was used to clarify the role of HMGB1 in cardiac I/R injury. Methods and Results Rats underwent 30 min of left coronary artery occlusion followed by 60 min reperfusion. An intravenous injection of anti-HMGB1 mAb or control IgG was administered just before reperfusion. The infarct size was enlarged in the anti-HMGB1 mAb group in comparison with the control group (p<0.05). The treatment of anti-HMGB1 mAb significantly increased the plasma troponin-T and norepinephrine (NE) content in the heart in comparison with the control (p<0.05). Moreover, the production of dihydroxyphenylglycol was reduced in the anti-HMGB1-treated group (p<0.05). Conclusion This study shows for the first time the effects of treatment with neutralizing anti-HMGB1 mAb on I/R injury in the rat heart. The findings support the novel view that I/R-induced HMGB1 may be an important factor in the modulation of interstitial NE. (Circ J 2008; 72: 1178 - 1184)<br>

収録刊行物

• Circulation Journal

  Circulation Journal 72 (7), 1178-1184, 2008

  一般社団法人 日本循環器学会

キーワード

• Coronary ischemia-reperfusion injury
• HMGB1
• Norepinephrine

詳細情報

• CRID: 1390001205101939584
• NII論文ID: 110006792076
• NII書誌ID: AA11591968
• DOI: 10.1253/circj.72.1178
• ISSN: 13474820
• ISSN: 13469843
• Web Site: http://www.jstage.jst.go.jp/article/circj/72/7/72_7_1178/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2008362009
• 本文言語コード: en
• データソース種別:
  • JaLC
  • Crossref
  • CiNii Articles
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