| Project/Area Number |
26461261
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Juntendo University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
富野 康日己 順天堂大学, 医学部, 名誉教授 (60130077)
鈴木 祐介 順天堂大学, 医学(系)研究科(研究院), 教授 (70372935)
菅谷 健 順天堂大学, 医学部, 非常勤講師 (40381561)
小林 敬 順天堂大学, 医学部, 助教 (70459056)
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| Research Collaborator |
TAKAHASHI Keiko 順天堂大学, 腎臓内科, 非常勤助手
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 酸化ストレス / 中大脳動脈虚血再灌流 / 腎交感神経 / L-FABP |
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| Outline of Final Research Achievements |
To investigate the roles of sympathetic nerve system (SNS) and oxidative stress in cerebro-cardio-renal syndrome (CRS), we developed cerebral ischemia/ reperfusion (IR) model and evaluated the impacts of renal sympathetic nerve denervation (RD) or an endogenous inhibitor for oxidative stress, L-FABP overexpression on this model. Unexpectedly, pretreatment of RD rather tended to enhance the mortality and infarction area after IR, suggesting that SNS could play an important role in maintaining the blood flow as well as the homeostasis in the acute phase of IR. We are now investigating the detail involvements of SNS activation in acute/ chronic phase of IR by modulating the timing of RD in the IR model.
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