| Project/Area Number |
13470323
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Kumamoto University |
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Principal Investigator |
USHIJIMA Kazuo Kumamoto University, Kumamoto University Hospital, Associate Professor, 医学部附属病院, 助教授 (60136752)
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| Co-Investigator(Kenkyū-buntansha) |
ARAKI Kimi Kumamoto University, Institute of Molecular Embryology and Genetics, Associate Professor, 発生医学研究センター, 助教授 (90211705)
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| Project Period (FY) |
2001 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥14,000,000 (Direct Cost: ¥14,000,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2002: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2001: ¥8,900,000 (Direct Cost: ¥8,900,000)
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| Keywords | ischemic neuronal death / gene trapping / neuroprotective agents / neuronal stem cells / glutamate / dantrolene / propofol / ulinastatin / 遅発性神経細胞死 |
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| Research Abstract |
We have isolated some unknown genes expressed in the mouse hippocampal CA1 region using a gene trapping method. The function of these genes has been analyzed in the mouse transient cerebral ischemic model, i.e., ligation of bilateral common carotid arteries. Moreover, the gene products are going to be induced into the brain with the use of protein transduction method to determine the functions in ischemia. In the future, more unknown genes related to neuronal injury and protection will be isolated. With regard to treatment of post-ischemic brain injury, we investigated the drugs already used in clinical practice. Then we reported that dantrolene and propofol could reduce the post-ischemic delayed neuronal death in the hippocampal CA1 sub field, and that the neuroprotection is caused by not only the decrease of extracellular glutamate but also antioxidative effects. Furthermore, massive intracerebroventricular ulinastatin, a human urine-derived trypsin inhibitor, could reduce the infarct volume in the rat focal ischemic model of middle cerebral artery occlusion. We are going to study the neuro-protective effects of various agents such as free radical scavengers and anesthetics. Great attention has been paid to the action of neural stem cells, ependymal cells in the subventricular zone, in ischemic brain damage. We demonstarted that ependymal cells migrate, proliferate, and differentiate in response to focal cerebral ischemia in rat model of middle cerebral artery occlusion. In relation to this interesting phenomenon, we are investigating the participation of genes.
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