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  1. C100 医学部/医学系研究科
  2. C100a 雑誌掲載論文
  3. 学術雑誌

Establishment of a mouse model of enalapril-induced liver injury and investigation of the pathogenesis

http://hdl.handle.net/2237/27027
http://hdl.handle.net/2237/27027
e1ff7ed8-16aa-4fca-8274-b4d3c0bfb518
名前 / ファイル ライセンス アクション
Establishment_of_a_mouse_model_of_enalapril-induced_liver_injury_and_investigation_of_the_pathogenesis.pdf Establishment_of_a_mouse_model_of_enalapril-induced_liver_injury_and_investigation_of_the_pathogenesis.pdf ファイル公開:2018/01/01 (5.0 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2017-10-10
タイトル
タイトル Establishment of a mouse model of enalapril-induced liver injury and investigation of the pathogenesis
言語 en
著者 Shirai, Yuji

× Shirai, Yuji

WEKO 73756

en Shirai, Yuji

Search repository
Oda, Shingo

× Oda, Shingo

WEKO 73757

en Oda, Shingo

Search repository
Makino, Sayaka

× Makino, Sayaka

WEKO 73758

en Makino, Sayaka

Search repository
Tsuneyama, Koichi

× Tsuneyama, Koichi

WEKO 73759

en Tsuneyama, Koichi

Search repository
Yokoi, Tsuyoshi

× Yokoi, Tsuyoshi

WEKO 73760

en Yokoi, Tsuyoshi

Search repository
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
抄録
内容記述 Drug-induced liver injury (DILI) is a major concern in drug development and clinical drug therapy. Since the underlying mechanisms of DILI have not been fully understood in most cases, elucidation of the hepatotoxic mechanisms of drugs is expected. Although enalapril (ELP), an angiotensin-converting enzyme inhibitor, has been reported to cause liver injuries with a low incidence in humans, the precise mechanisms by which ELP causes liver injury remains unknown. In this study, we established a mouse model of ELP-induced liver injury and analyzed the mechanisms of its hepatotoxicity. Mice that were administered ELP alone did not develop liver injury, and mice that were pretreated with a synthetic glucocorticoid dexamethasone (DEX) and a glutathione synthesis inhibitor l-buthionine-(S,R)-sulfoximine (BSO) exhibited liver steatosis without significant increase in plasma alanine aminotransferase (ALT). In mice pretreated with DEX and BSO, ALT levels were significantly increased after ELP administration, suggesting that hepatic steatosis sensitized the liver to ELP hepatotoxicity. An immunohistochemical analysis showed that the numbers of myeloperoxidase-positive cells that infiltrated the liver were significantly increased in the mice administered DEX/BSO/ELP. The levels of oxidative stress-related factors, including hepatic heme oxygenase-1, serum hydrogen peroxide and hepatic malondialdehyde, were elevated in the mice administered DEX/BSO/ELP. The involvement of oxidative stress in ELP-induced liver injury was further supported by the observation that tempol, an antioxidant agent, ameliorated ELP-induced liver injury. In conclusion, we successfully established a model of ELP-induced liver injury in DEX-treated steatotic mice and demonstrated that oxidative stress and neutrophil infiltration are involved in the pathogenesis of ELP-induced liver injury.
言語 en
内容記述タイプ Abstract
出版者
言語 en
出版者 nature
言語
言語 eng
資源タイプ
資源タイプresource http://purl.org/coar/resource_type/c_6501
タイプ journal article
出版タイプ
出版タイプ AM
出版タイプResource http://purl.org/coar/version/c_ab4af688f83e57aa
DOI
関連タイプ isVersionOf
識別子タイプ DOI
関連識別子 https://doi.org/10.1038/labinvest.2017.22
ISSN
収録物識別子タイプ PISSN
収録物識別子 0023-6837
書誌情報 en : Laboratory Investigation

巻 97, p. 833-842, 発行日 2017-07
著者版フラグ
値 author
URI
識別子 http://doi.org/10.1038/labinvest.2017.22
識別子タイプ DOI
URI
識別子 http://hdl.handle.net/2237/27027
識別子タイプ HDL
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