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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
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
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
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.
キーワード
ischemia/reperfusion injury
heme oxygenase
liver damage
living donor liver transplantation
発行日
2012-02
出版物タイトル
International Journal of Molecular Medicine
29巻
2号
出版者
Spandidos Publications Ltd.
開始ページ
135
終了ページ
140
ISSN
1107-3756
NCID
AA11445762
資料タイプ
学術雑誌論文
関連URL
http://ousar.lib.okayama-u.ac.jp/metadata/48436
言語
English
OAI-PMH Set
岡山大学
論文のバージョン
publisher
DOI
PubMed ID