| Project/Area Number |
09470157
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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 |
Neurology
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| Research Institution | Tokai University |
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Principal Investigator |
SHINOHARA Yukito Tokai University, school of Medicine, Professor, 医学部, 教授 (60051504)
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| Co-Investigator(Kenkyū-buntansha) |
TAKIZAWA Syunya Tokai University, school of Medicine, Assistant Professor, 医学部, 講師 (70197234)
MATSUSHIMA Kazushi Tokai University, school of Medicine, Instructor, 医学部, 助手 (70209542)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥4,000,000 (Direct Cost: ¥4,000,000)
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| Keywords | ischemia / antisense oligodeoxynucleotide / Bax / p53 / neuroprotection / apoptosis / global ischemia / focal cerebral ischemia / Antisense oligodeoxy nucleotide / P^<53> / Apoptosis |
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| Research Abstract |
Abstract
To elucidate the mechanism of delayed neuronal death after global ischemia, we studied the expression of Bax and neuroprotoction using antisense oligodeoxynucleotide (antisense) designed to block translation of Bax mRNA.Antisense was infused into left lateral ventricle. lachemia was induced by the two-vessel occlusion method with hypotensiora. Bax expression was studied by immunohistochemistry at 2 days after infusion. Neuroprotection was studied counting surviving neurons in the hippocampus CA1 at 7 days after ischemia. Bat expreBsion was not significantly decreased in the antisense group compared to the sense or vehicle groups. But cell death in the hippocampus CA1 was showing a tendency to decrease in the antisense group compared with the sense or vehicle groups. These findings provide evidence to support the role of apoptosis in delayed neuronal death. We need further study to know exact molecular mechanisms of neuronal cell death secondary to ischemia.
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