| Project/Area Number |
07671508
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Cerebral neurosurgery
|
|---|
| Research Institution | Nagoya University |
|---|
Principal Investigator |
INAO Suguru Nagoya University, School of Medicine, Assistant professor, 医学部, 講師 (20151566)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
口脇 博治 名古屋大学, 医学部, 講師 (60135340)
|
|---|
| Project Period (FY) |
1995 – 1997
|
| Project Status |
Completed (Fiscal Year 1997)
|
| Budget Amount *help |
¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1996: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
|
|---|
| Keywords | brain / glia / GFAP / immunohistochemistry / injury / intercellular adhesion molecule-1 / interleukin-1 / 細胞間接着因子 / グリア / インターロイキン-1 / ベータアミロイド蛋白 / プレカーサーベータアミロイド蛋白 / 凍結損傷 |
|---|
| Research Abstract |
The macrophage and astrocyte are activated in the local area after brain injury via the humoral stimulations of the biologically active substances such as the cytokines and nerve growth factors. Rat brains were immunostained for GFAP,ED-1, PCNA in the various experimental times up to 14 days after brain injury and microscopically examined. Reactive astrogliosis after brain injury initiated just after injury and showed maximum at 5 days post-injury. IL-1 promotes glia to express ICAM-1 in vivo. ICAM-1-immunopositive glia began to emerge around the wound and reached a maxium at 2 days, persisted until 7 days post-injury. A neutralizing monoclonal antibody against IL-1 beta was infused into the wound immediately following the injury. This treatment resulted in a significant reduction of ICAM-1-positive glia at 1 and 2 days post-injury. IL-1 beta affects ICAM-1 expression on glia in vivo after experimental brain injury. We conclude that the biologically active substances play an important role in the healing phase following CNS injury.
|
