2000 Fiscal Year Final Research Report Summary
Analysis of apoptosis-related products in delayed neuronal death following cerebral ischemia
| Project/Area Number |
10557129
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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 | 展開研究 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Saga Medical School |
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Principal Investigator |
TABUCHI Kazuo Saga medical school, Neurosurgery, Professor, 医学部, 教授 (50116480)
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| Co-Investigator(Kenkyū-buntansha) |
FURUTA Makoto Saga medical school, Neurosurgery, Instructor, 医学部, 助手 (20325608)
SHIRAISHI Tetsuya Saga medical school, Neurosurgery, Assistant professor, 医学部, 講師 (70206275)
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| Project Period (FY) |
1998 – 2000
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| Keywords | cerebral ischemia / apoptosis / SELDI-TOF MS / midkine / Bcl-2 / cerebrospinal fluid |
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| Research Abstract |
We examined the internucleosomal DNA fragmentation by in situ DNA double breaks staining and immunohistochemical expression of Bcl-2 family gene products in rat hippocampal CA1 pyramidal neurons following transient ischemia (rat 4-ressels occlusion model). The degenerating dark neurons with condensed nuclei in CA1 were clearly stained for DNA strand breaks 2 days ischemia. Apoptotic indices which stand for percentage of positive stained nuclei in total nuclei were as follows ; O (Sham), 9.2 (Day 1), 68.2 (Day 2), 93.5 (Day4). Bcl-2α expression was observed in both CA1 and CA3 of sham-operated rats. However, positivity of Bcl-2 was decreated in CA1 and was increased in CA3 of ischemia rats, On the other hand, no staining of Bcl-xL in sham-operated group and positive staining in other group were demonstrated. No positive staining of Bax was observed in any groups. These results suggested that Bcl-2 gene products might be involved in apoptotic neuronal death in CA1 after transient ischemia.
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