Ischemic Neuronal Damade and heat Shock (Stress) Protein
Project/Area Number |
02670635
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Cerebral neurosurgery
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Research Institution | Nagoya City University |
Principal Investigator |
MABE Hideo Nagoya City University, Department of Neurosurgery, Assistant Professor, 医学部, 助教授 (20093073)
|
Co-Investigator(Kenkyū-buntansha) |
KANAI Hideki Nagoya City University, Department of Neurosurgery, Assistant, 医学部, 助手 (90185893)
NAGAI Hajime Nagoya City University, Department of Neurosurgery, Professor, 医学部, 教授 (00023747)
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Project Period (FY) |
1990 – 1991
|
Project Status |
Completed (Fiscal Year 1991)
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Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1991: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1990: ¥1,400,000 (Direct Cost: ¥1,400,000)
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Keywords | Heat shock protein 70 / ischemic neuronal damage / Hyperthermia / Ischemic tolerance / Rat |
Research Abstract |
We investigated the possibility that neuronal cells given a hyperthermic or mild ischemia treatment acquired tolerance to a subsequent, and what would be lethal, ischemic stress in vivo. Hyperthermia was produced in the rat by placing them in a water bath maintained at 42゚ C. The body temperature of the rat was raised to 42゚ C for 15 min and then the animals were subjected to 15 min of four-vessel occlusion. Seven days after recirculation, the animals were sacrificed, and the brains were removed, fixed in 10% formalin and stained by hematoxylin-eosin for histopathology. In the rat subjected to 15 min of four-vessel occlusion 8 or 24 hours after hyperthermia, ischemic neuronal change in the CA1 was less compared to 15 min of four-vessel occlusion without hyperthermia. The hippocampus from animals subjected to hyperthermia was analysed using immunoblotting. Expression of heat shock proteon 70(HSP 70)was shown in the animals 8 or 24 hours after hyperthermia. Eight min ischemia 24 hours before 15 min ischemia exhibited protective effect against ischemic neuronal change. Expression of HSP 70 was shown in the hippocampus 24 hours after 8 min ischemia, but was not after 15 min ischemia. These results provides support for the possibility that hyperthermia or mild ischemia makes the neuronal cells more resistant to the ischemic damage. It is suggested that these tolerance to the ischemic stress correlates to expression of HSP 70.
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Report
(3 results)
Research Products
(4 results)