| Project/Area Number |
09671457
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Cerebral neurosurgery
|
|---|
| Research Institution | KINKI UNIVERSITY |
|---|
Principal Investigator |
AKAI Fumiharu KINKI UNIVERSITY, SCHOOL OF MED., 医学部, 講師 (40122006)
|
|---|
| 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)
|
|---|
| Project Period (FY) |
1997 – 1999
|
| Project Status |
Completed (Fiscal Year 1999)
|
| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥1,600,000 (Direct Cost: ¥1,600,000)
|
|---|
| Keywords | ISCHEMIA / SPINAL CORD / DDC / NEURONAL DEATH / APOPTOSIS / SHR |
|---|
| 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.
|
