| Project/Area Number |
08457602
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
NOMURA Yasuyuki Hokkaido Univ. Fac. of pharmac. Sci. Prof., 薬学部, 教授 (00034041)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥8,700,000 (Direct Cost: ¥8,700,000)
Fiscal Year 1997: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1996: ¥7,300,000 (Direct Cost: ¥7,300,000)
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| Keywords | brain ischemia / neuronal apoptosis / glial cells / cytokine / 胸腺細胞 / リンパ球 / アセチルコリン受容体 / カルシトニン / 核内転写因子 |
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| Research Abstract |
Inflammatory/immnological processes underlie survival/damage of meurons after brain ischemia. It is not clear whether or not the neuronal death after brain ischemia is apoptosis or necrosis. Under the condition of transient forebrain ischemia, we obtained results suggesting apoptosis in the delayd neuronal death of the CA1 pyramidal neurons.
In glia ; cells, cytokines such as IL-1beta asnd TNF-alpha are produced following ischemic stresses. On the other hand, it is suggested that NO/iNOS is involved in neuronal apoptosis. The iNOS induction was detected primarily in astrocytes after the transient forebrain ischemia when the neuronal apoptosis was observed. In the[next series, we examined whether cytokines and chemokines were produced after the brain ischemia. The transient expressions of mRNA of IL-6 and CINC were observed after the transient forebrain ischemia in the cerebral cortex and the hippocampus. IL-6 is known as a survival factor for neurons. It is, therefore, suggested that IL-6 may play a role as a protective factor against ischemic stress. The precise roles of NO,cytokines and chemokines on brain ischemic insult are an interesting subject to be elucidated.
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