| Project/Area Number |
18591725
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
MUROZONO Michihiro Tokyo Medical University, School of Medicine, Assistant Professor (70276947)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUMOTO Shohei Tokyo Medial University, School of Medicine, Assistant Professor (30256250)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,190,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥390,000)
Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2006: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Brain ischemia / P-glycoprotein / blood-brain barrier |
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| Research Abstract |
We measured apoptotic factors, cytokines and factors for tissue repair for the evluation of postischemic influence of P-gp by using immunohistochemistry, western blotting, and ELISA this time. In addition ; we investigated how mdrla P-gp existing in brain of normal mice changed compared with that of mdrla knockout mice. In mdrla knockout mice, Bcl-2 was more and bax was less after ischemia than those of wild-type mice significantly.
Therefore, antiapoptosis action strongly worked on the mdrla ko mouse in comparison with wild-type mice on brain ischemia. After transient cerebral ischemia, on wild-type mice p-gp expressed contineously and without decreaseing, so it is possible that p-gp can act as apotosis inducer at the early stage on brain ischemia.
On the other hand, by a combined medication of cyclosporiti A and Ondansetron, damage of cerebral ischemia decreased significantly. From the above, it is suggested that when it uses cerebroprotection agent which depends on P-gp for treatment for cerebral ischemia, it does a cerebroprotection effect effectively to use other materials dependent on P-gp together.
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