| Project/Area Number |
20591806
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
|
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| Research Institution | Yamaguchi University |
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Principal Investigator |
FUKUDA Shiro Yamaguchi University, 大学院・医学系研究科, 講師 (70322245)
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|---|
| Co-Investigator(Kenkyū-buntansha) |
MATSUMOTO Mishiya 山口大学, 大学院・医学系研究科, 教授 (60243664)
ISHIDA Kazuyoshi 山口大学, 医学部付属病院, 講師 (80314813)
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| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | AMP-activated Protein Kinase / 脳虚血 / ラット / AICAR / compound C / AMP-activated rotein kinase / 細胞内エネルギー調節 / 前脳虚血 / 海馬 / 遅発性神経細胞傷害 / AMP-ativated protein kinase / 中大脳動脈閉塞モデル / TTC染色 / 神経細胞傷害 / ウィスターラット / 脳・神経 / 虚血性細胞障害 / 細胞内代謝調節 / 免疫ブロット法 / ラット断頭モデル / 全脳虚血 |
|---|
| Research Abstract |
The tendency of increasing in p-AMPKα2 and p-AMPKβ1 was observed in the brain samples 60 minutes after decapitation of rats. This result suggested that AMPK was activated by neuronal ischemia. Infarction volumes in focal ischemia with rat model were decreased by AICAR, which is one of the activators of AMPK. However, AICAR exacerbated neuronal damage in gerbil forebrain ischemia, and the same exacerbation was observed in the administration of Compound C, one of the AMPK inhibitors.
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