Identification of the genes in the ischemic neuronal cell death
| Project/Area Number |
16591446
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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 |
Cerebral neurosurgery
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| Research Institution | Nagasaki University |
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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)
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| 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)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| 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)
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| Keywords | vitamin E / HT-22 / neuronal cell death / glutamate / COX-2 |
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| 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.
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Report
(3 results)
Research Products
(2 results)
