ID | 47583 |
フルテキストURL | |
著者 |
Matsumi, Junya
Department of Anesthesiology and Resuscitology, Okayama University Medical School
Morimatsu, Hiroshi
Department of Anesthesiology and Resuscitology, Okayama University Medical School
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Matsusaki, Takashi
Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kaku, Ryuji
Department of Anesthesiology and Resuscitology, Okayama University Medical School
Shimizu, Hiroko
Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Takahashi, Toru
Faculty of Health and Welfare Science, Okayama Prefectural University
Yagi, Takahito
Department of Hepato-Biliary-Pancreatic Surgery, Okayama University Medical School
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Matsumi, Masaki
Department of Anesthesiology and Resuscitology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Morita, Kiyoshi
Department of Anesthesiology and Resuscitology, Okayama University Medical School
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抄録 | Living donor liver transplantation (LDLT) requires ischemia/reperfusion (I/R), which can cause early graft injury. However, the detailed mechanism of I/R injury remains unknown. Heme oxygenase-1 (HO-1) is a rate-limiting enzyme in heme catabolism and results in the production of iron, carbon monoxide (CO), and biliverdin IXα. Furthermore, in animals, HO-1 has a protective effect against oxidative stress associated with I/R injury. However, in humans, the molecular mechanism and clinical significance of HO-1 remain unclear. We previously demonstrated that exhaled CO levels increase during LDLT, and postulated that this may indicate I/R injury. In this study, we elucidate the origin of increased exhaled CO levels and the role of HO-1 in I/R injury during LDLT. We studied 29 LDLT donors and recipients each. For investigation of HO-1 gene expression by polymerase chain reaction and HO-1 localization by immunohistological staining, liver biopsies from the grafted liver were conducted twice, once before and once after I/R. Exhaled CO levels and HO-1 gene expression levels significantly increased after I/R. In addition, HO-1 levels significantly increased after I/R in Kupffer cells. Furthermore, we found a significant positive correlation between exhaled CO levels and HO-1 gene expression levels. These results indicated that increased heme breakdown in the grafted liver is the source of increased exhaled CO levels. We also found a significant relationship between HO-1 gene expression levels and alanine aminotransferase (ALT) levels; i.e., the higher the HO-1 gene expression levels, the higher the ALT levels. These results suggest that HO-1-mediated heme breakdown is caused by I/R during LDLT, since it is associated with increased exhaled CO levels and liver damage.
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キーワード | ischemia/reperfusion injury
heme oxygenase
liver damage
living donor liver transplantation
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発行日 | 2012-02
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出版物タイトル |
International Journal of Molecular Medicine
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巻 | 29巻
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号 | 2号
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出版者 | Spandidos Publications Ltd.
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開始ページ | 135
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終了ページ | 140
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ISSN | 1107-3756
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NCID | AA11445762
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資料タイプ |
学術雑誌論文
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関連URL | http://ousar.lib.okayama-u.ac.jp/metadata/48436
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言語 |
英語
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論文のバージョン | publisher
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DOI | |
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