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

• DOI: 10.1371/journal.pone.0196191
• Publication Date: 2018-04-24T13:28:24Z
• Authors: Takeaki Shinjo; Tatsuhide Tanaka; Hiroaki Okuda; Akira T. Kawaguchi; Kentaro Oh-hashi; Yuki Terada; Ayami Isonishi; Shoko Morita-Take...; Kouko Tatsumi; Masahiko Kawaguchi; Akio Wanaka
• Keywords: Cytoprotection

Oxidative stress contributes to myocardial ischemia-reperfusion injury, which causes cardiomyocyte death and precipitate life-threatening heart failure. Propofol has been proposed protect cells or tissues against oxidative stress. However, the mechanisms underlying its beneficial effects are not fully elucidated. In present study, we employed an in vitro injury model, rat cardiac H9c2 were treated with H2O2, investigated roles of propofol treatment reduced H2O2-induced apoptotic cell death. While H2O2 induced expression antioxidant enzyme HO-1, further increased HO-1 mRNA protein levels. also promoted nuclear localization Nrf2 presence H2O2. Knockdown using siRNA suppressed propofol-inducible Nrf2-downstream enzyme. propofol-induced cytoprotection. addition, overexpression expression. These results suggest that exerts antioxidative by inducing downstream cells. Finally, examined effect on cardiomyocytes models. The level was at 15 min after reperfusion group compared penumbra region. protects from via Nrf2/HO-1 cascade.