| Project/Area Number |
23592094
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Nagasaki University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TAKESHITA Tomonori 長崎大学, 大学病院, 医員 (30597365)
TOYODA Keisuke 長崎大学, 大学病院, 医員 (40597366)
BABA Shiro 長崎大学, 大学病院, 助教 (30530430)
IZUMO Tsuyoshi 長崎大学, 大学病院, 助教 (40343347)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 脳血管障害 / 血液脳関門 / 血管原性脳浮腫 / blood brain barrier / hypertension / glioma / hyperglicemia / ラット |
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| Research Abstract |
We used in vitro blood-brain barrier (BBB) models with primarily cultured BBB-related cells from rats. Treatment of AGEs did not affect the transendothelial electrical resistance (TEER) in the BBB model under normoxia, but there was a significant decrease in TEER under 3-h oxygen glucose deprivation (OGD)/24-h reoxygenation conditions with AGEs. Cilostazol inhibited decreases in TEER induced by 3-h OGD/24-h reoxygenation with AGEs. Furthermore, while AGEs increased the production of extracellular transforming growth factor (TGF)-beta1, cilostazol inhibited the production of extracellular TGF- beta 1 and restored the integrity of tight junctions.
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