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Please use this identifier to cite or link to this item: http://hdl.handle.net/10564/3544

Title: Propofol induces nuclear localization of Nrf2 under conditions of oxidative stress in cardiac H9c2 cells.
Other Titles: 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
Authors: Shinjo, Takeaki
Tanaka, Tatuhide
Okuda, Hiroaki
Kawaguchi, Akira
Oh-Hashi, Kentaro
Terada, Yuki
Isonishi, Ayako
Morita-Takemura, Shoko
Tatsumi, Kouko
Kawaguchi, Masahiko
Wanaka, Akio
Issue Date: 24-Apr-2018
Publisher: Public Library of Science
Citation: PloS one Vol.13 No.4 Article No.e0196191 (2018 Apr)
Abstract: 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.
Description: 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.
URI: http://hdl.handle.net/10564/3544
ISSN: 19326203
Academic Degrees and number: 24601A696
Degree-granting date: 2019-03-15
Degree name: 博士(医学)
Degree-granting institutions: 奈良県立医科大学
Appears in Collections:2018年度

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