| Project/Area Number |
16591811
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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 |
Emergency medicine
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| Research Institution | Oita University |
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Principal Investigator |
IWASAKA Hideo Oita University, 医学部, Associate Professor (90175216)
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| Co-Investigator(Kenkyū-buntansha) |
KITANO Takaaki Oita University, 医学部, Associate Professor (20211196)
UNOSHIMA Masako Oita University, 医学部, Teaching Fellow (90336256)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2006: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2005: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Cerebeal ischemic reperfusion injury / UCP-2 / ethyl pyruvate / apoptosis / mitochondria / HMGB1 |
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| Research Abstract |
The most important end points of cardiopulmonary resuscitaion is cerebral resuscitation. We evaluate the new molecular therapeutic approach targeting to mitochondria in rat cerebral ischemic reperfusion model. The uncoupling protein 2(UCP-2) is a transporter, presents in the mitochondrial inner membrane, that mediate a regulated discharge of the proton gradient that is generated by the respiratory chain. We found that UCP-2 can be induced thermal stress (rectal temperature 42℃ for 15 minutes). UCP-2 preinduced rat can survive more longer than control group in cerebral ischemia reperfusion model. This mechanisms are mediated reduced production of HMGB1 and inhibition of apoptosis. Ethyl pyruvate, a simple derivative of the parent compound, is thought to be more stable. Ringer's ethyl pyruvate solution has is evaluated in cerebral ischemic reperfusion model. Treatment with ethyl pyruvate solution is shown to be able to improve survival and decrease brain injury compared with treatment with Ringer's lactate solution. This mechanisms are mediated energy supply, reduced production of free radicals and reduced apoptosis. HMGB1 also plays important lethal mediator in cerebral ischemia reperfusion injury. UCP-2 treatment, ethyl pyruvate solution and HMGB1 therapeutic managements warrant further evaluation for the resuscitaion of patients with cerebral reperfusion injury.
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