| Project/Area Number |
26462154
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Neurosurgery
|
|---|
| Research Institution | University of Yamanashi |
|---|
Principal Investigator |
YAGI Takashi 山梨大学, 総合研究部, 助教 (90345702)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
吉岡 秀幸 山梨大学, 総合研究部, 助教 (20402076)
木内 博之 山梨大学, 総合研究部, 教授 (30241623)
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Keywords | neuroprotection / ischemic tolerance / neurovascular protection / ischemic preconditioning / 神経保護 / 虚血耐性現象 / アストロサイト |
|---|
| Outline of Final Research Achievements |
We investigated the involvement of Nrf2 / ARE signaling pathway and the neuroprotective mechanism of ischemic tolerance phenomenon using rat transient forebrain ischemia model. Following transient forebrain ischemia, expression of Nrf2 was observed in neuronal cells, astrocytes, and microglial cells, and the expression kinetics differed between lethal ischemia and non-lethal ischemia . In the ischemia tolerance model, the expression of Nrf2 tended to be amplified and maintained over a long period of time.
It was suggested that the neuroprotective mechanism of the ischemic tolerance phenomenon may involve the activation of the Nrf2 pathway of glial cells in addition to the intrinsic protective mechanism of neuronal cells.
|
