| Project/Area Number |
16591446
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Cerebral neurosurgery
|
|---|
| Research Institution | Nagasaki University |
|---|
Principal Investigator |
MATSUO Takayuki Nagasaki University, Hospital of Medicine and Dentistry, Lecturer, 医学部・歯学部附属病院, 講師 (00274655)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
KITAGAWA Naoki Nagasaki University, Hospital of Medicine and Dentistry, Lecturer, 医学部・歯学部附属病院, 講師 (30253652)
|
|---|
| Project Period (FY) |
2004 – 2005
|
| Project Status |
Completed (Fiscal Year 2005)
|
| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥2,200,000 (Direct Cost: ¥2,200,000)
|
|---|
| Keywords | vitamin E / HT-22 / neuronal cell death / glutamate / COX-2 |
|---|
| Research Abstract |
The accumulation of damage caused by oxidative stress exacerbates cell death in many neurodegenerative diseases. We evaluated the mechanism of neuronal cell death raised by glutamate-induced toxicity using the immortalized mouse hippocampal cell line HT-22. Our results showed that vitamin E prevented glutamate-induced cell death, accompanied by the decline of COX-2 expression confirmed by RT-PCR and immunocytochemistry. Moreover, the neuroprotection was still effective even if vitamin E was supplied after glutamate treatment. The decline of COX-2 activity was also highly correlated with the neural protective effect against glutamate-induced toxicity. These results represent new insights about the timing of vitamin E supplementation after toxic stimulation and one mechanism by which vitamin E could prevent neuronal cell death by controlling COX-2 activity.
|
