1999 Fiscal Year Final Research Report Summary
SPINAL ISCHEMIA, ITS MECHANISM AND STRATEGY OF TREATMENT-A NEW MODEL AND GLIAL REACTION AND INDUCTION
| Project/Area Number |
09671457
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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 | KINKI UNIVERSITY |
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Principal Investigator |
AKAI Fumiharu KINKI UNIVERSITY, SCHOOL OF MED., 医学部, 講師 (40122006)
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| Co-Investigator(Kenkyū-buntansha) |
NISHIDA Syouzou KINKI UNIVERSITY, SCHOOL OF PHARM.., 薬学部, 講師 (40208187)
TANEDA Mammoru KINKI UNIVERSITY, SCHOOL OF MED, PROF., 医学部, 教授 (10236713)
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| Project Period (FY) |
1997 – 1999
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| Keywords | ISCHEMIA / SPINAL CORD / DDC / NEURONAL DEATH / APOPTOSIS / SHR |
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| Research Abstract |
1) The light and electron microscopic localization of single strand DNA protein, a marker of apoptosis was studied. Immunoreaction was recognized in the nucleus without morphological changes 1 day after ischemic insult. Degradation of single strand DNA can occur during delayed neuronal death, preceding the appearance of double strand DNA breaks.(Neurosci Lett 240 : 69, 1998)
2) DDC induced apoptosis in a morphological nature in PC12 cells, and led to down -regulation of Cu/Zn-SOD activity, then reduced intracellular HィイD22ィエD2OィイD22ィエD2. A hypoxia prevented the cells from DDC-induced apoptosis. These data confirmed OィイD22ィエD2 induced apoptosis in PC12 cells. Nitro-oxide-synthetase, Fe-chelator did not prevent the apoptosis.
Peroxinitrate and also OH did not contribute DDC-induced apoptosis. NGF and NAC protected the apoptosis. DDC did not activate NF-kB. We concluded that NAC reduced DDC-induced apoptosis by interception of an unknown direct signal pathway, by which OィイD22ィエD2 induced apoptosis.
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