1998 Fiscal Year Final Research Report Summary
Molecular analysis for ischemic tolerance of neuron
| Project/Area Number |
09671422
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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 | KYOTO UNIVERSITY |
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Principal Investigator |
NOZAKI Kazuhiko KYOTO UNIVERSITY,Medical school Dept of Neurosurg assistant prof., 医学研究科, 講師 (90252452)
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| Co-Investigator(Kenkyū-buntansha) |
HOSHIMARU Minoru Otsu Red Cross Hospital, 大津市民病院, 脳神経外科
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| Project Period (FY) |
1997 – 1998
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| Keywords | Ischemic tolerance / neuron / molecular biology / rat / gerbil / mouse |
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| Research Abstract |
The mechanisms of neuronal death and survival in ischemic brain are one of major topics in neuroscience. Recent papers have stressed the important role of mitochondria in ischemic neuronal damage in that both necrosis and apoptosis are induced by the dysfunction of mitochondria. On the other hand, the induction of ischemic tolerance in neuron after ischemic stress has been reported, but the molecular mechanisms of ischemic tolerance have not been elucidated. In the present study, we used several cerebral ischemic models including a. transient forebrain ischemia in gerbil, b. 3-nitropropionic acid-induced striatal damage in rat, c. permanent middle cerebral artery occlusion in rat, d. transient middle cerebral artery occlusion in rat, e. permanent middle cerebral artery occlusion in mouse in order to examine the relation of mitochondrial function and apoptosis and the mechanism of ischemic tolerance. We have demonstrated that apoptosis was involved in neuronal death in model a and b, that apoptosis related genes and poly(ADP-ribosyl)ation was involved in neuronal damage in model b and c, that thioredoxin is markedly induced in neuron in ischemic penumbra in model c and d, and that chemical preconditioning with 3-nitropropionic acid and overexpression of thioredoxin can induce ischemic tolerance in model a and e.
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