Effects of HMGB1 on Ischemia-Reperfusion Injury in the Rat Heart
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- Oozawa Susumu
- Department of Cardiovascular Surgery, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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- Mori Shuji
- School of Pharmacy, University of Shujitsu
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- Kanke Toru
- Department of Pharmacology, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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- Takahashi Hideo
- Department of Pharmacology, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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- Liu Keyue
- Department of Pharmacology, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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- Tomono Yasuko
- Shigei Medical Institute
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- Asanuma Masato
- Department of Brain Science, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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- Miyazaki Ikuko
- Department of Brain Science, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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- Nishibori Masahiro
- Department of Pharmacology, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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- Sano Shunji
- Department of Cardiovascular Surgery, University of Okayama Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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Abstract
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>
Journal
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- Circulation Journal
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Circulation Journal 72 (7), 1178-1184, 2008
The Japanese Circulation Society
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Details 詳細情報について
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- CRID
- 1390001205101939584
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- NII Article ID
- 110006792076
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- NII Book ID
- AA11591968
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- ISSN
- 13474820
- 13469843
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- Text Lang
- en
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- Data Source
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- JaLC
- Crossref
- CiNii Articles
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- Abstract License Flag
- Disallowed