| Project/Area Number |
15K20058
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Anesthesiology
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| Research Institution | Nara Medical University |
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Principal Investigator |
Shinjo Takeaki 奈良県立医科大学, 医学部, 助教 (70624914)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 酸化ストレス / プロポフォール / 抗酸化酵素 / 細胞保護効果 / アポトーシス / NMBAs / アストロサイト / 神経伝達物質 |
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| Outline of Final Research Achievements |
We changed to a study to elucidate that propofol, an anesthetic sedative, protects against cell damage due to oxidative stress and protective intracellular signal. Propofol has been proposed to protect cells or tissues against oxidative stress. 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 suppressed the propofol-induced cytoprotection. These results suggest that propofol exerts antioxidative effects by inducing nuclear localization of Nrf2 and expression of its downstream enzyme in cardiac cells.
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