| 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)
戸田 啓介 佐賀医科大学, 医学部, 助手 (80274588)
福山 幸三 佐賀医科大学, 医学部, 講師 (60238516)
木原 俊一 佐賀医科大学, 医学部, 助手 (30253610)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥7,300,000 (Direct Cost: ¥7,300,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1999: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1998: ¥3,300,000 (Direct Cost: ¥3,300,000)
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| Keywords | cerebral ischemia / apoptosis / SELDI-TOF MS / midkine / Bcl-2 / cerebrospinal fluid / 虚血 / 神経細胞死 / Bcl-xL / 遅発性神経細胞死 / DNAfragmentation / TUNEL / Bax |
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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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