Propofol induces nuclear localization of Nrf2 under conditions of oxidative stress in cardiac H9c2 cells.

• 資料種別: 博士論文
• タイトル: Propofol induces nuclear localization of Nrf2 under conditions of oxidative stress in cardiac H9c2 cells.
• 著者・編者: Shinjo, Takeaki; Tanaka, Tatuhide; Okuda, Hiroaki; Kawaguchi, Akira; Oh-Hashi, Kentaro; Terada, Yuki; Isonishi, Ayako; Morita-Takemura, Shoko; Tatsumi, Kouko; Kawaguchi, Masahiko; Wanaka, Akio
• 著者標目: Shinjo, Takeaki; Tanaka, Tatuhide; Okuda, Hiroaki; Kawaguchi, Akira; Oh-Hashi, Kentaro; Terada, Yuki; Isonishi, Ayako; Morita-Takemura, Shoko; Tatsumi, Kouko; Kawaguchi, Masahiko; Wanaka, Akio
• 出版事項: Public Library of Science
• 出版年月日等: 2018-04-24
• 出版年（W3CDTF）: 2018-04-24
• 並列タイトル等: プロポフォールは、酸化的ストレス条件下で心筋細胞株H9c2におけるNrf2の発現及び核局在を誘導する
• タイトル（掲載誌）: PloS one
• 巻号年月日等（掲載誌）: 13 4
• 掲載巻: 13
• 掲載号: 4
• 掲載ページ: Article No.e0196191-
• ISSN（掲載誌）: ISSN : 1932-6203
• 授与機関名: 奈良県立医科大学
• 授与年月日: 2019-03-15
• 報告番号: 甲第696号
• 学位: 博士（医学）
• 本文の言語コード: eng
• 対象利用者: 一般
• 一般注記: type:Thesis; Oxidative stress contributes to myocardial ischemia-reperfusion injury, which causes cardiomyocyte death and precipitate life-threatening heart failure. Propofol has been proposed to protect cells or tissues against oxidative stress. However, the mechanisms underlying its beneficial effects are not fully elucidated. In the present study, we employed an in vitro oxidative injury model, in which rat cardiac H9c2 cells were treated with H2O2, and investigated roles of propofol against oxidative stress. Propofol treatment reduced H2O2-induced apoptotic cell death. While H2O2 induced expression of the antioxidant enzyme HO-1, propofol further increased HO-1 mRNA and protein levels. Propofol also promoted nuclear localization of Nrf2 in the presence of H2O2. Knockdown of Nrf2 using siRNA suppressed propofol-inducible Nrf2 and expression of Nrf2-downstream antioxidant enzyme. Knockdown of Nrf2 suppressed the propofol-induced cytoprotection. In addition, Nrf2 overexpression induced nuclear localization of Nrf2 and HO-1 expression. These results suggest that propofol exerts antioxidative effects by inducing nuclear localization of Nrf2 and expression of its downstream enzyme in cardiac cells. Finally, we examined the effect of propofol on cardiomyocytes using myocardial ischemia-reperfusion injury models. The expression level of Nrf2 protein was increased at 15 min after reperfusion in the ischemia-reperfusion and propofol group compared with ischemia-reperfusion group in penumbra region. These results suggest that propofol protects cells or tissues from oxidative stress via Nrf2/HO-1 cascade.; 博士（医学）・甲第696号・平成31年3月15日; Copyright: © 2018 Shinjo et al. This is an open access article distributed under the terms of the Creative Commons Attribution License(https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.; identifier:PloS one Vol.13 No.4 Article No.e0196191 (2018 Apr); identifier:19326203; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/3544; identifier:PloS one, 13(4): Article No.e0196191
• オンライン閲覧公開範囲: インターネット公開
• 関連情報（DOI）: 10.1371/journal.pone.0196191
• 連携機関・データベース: 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• 提供元機関・データベース: 奈良県立医科大学 : 奈良県立医科大学機関リポジトリ GINMU

目次

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3544/1/01%e7%94%b2696%e6%9c%ac%e6%96%87%e3%81%ae%e8%a6%81%e6%97%a8.pdf fulltext

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3544/2/02%e7%94%b2696%e5%af%a9%e6%9f%bb%e8%a6%81%e6%97%a8.pdf fulltext

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/3544/3/03%e7%94%b2696%e6%9c%ac%e6%96%87.pdf fulltext