| Project/Area Number |
24659072
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Medical pharmacy
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| Research Institution | University of Toyama |
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Principal Investigator |
HOSOYA Ken-ichi 富山大学, 大学院医学薬学研究部(薬学), 教授 (70301033)
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| Co-Investigator(Kenkyū-buntansha) |
KUBO Yoshiyuki 富山大学, 大学院医学薬学研究部(薬学), 准教授 (20377427)
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| Co-Investigator(Renkei-kenkyūsha) |
TACHIKAWA Masanori 東北大学, 大学院薬学研究科, 准教授 (00401810)
AKANUMA Shin-ichi 富山大学, 大学院医学薬学研究部(薬学), 助教 (30467089)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | プロスタグランジン / 血液脳関門 / 脳内炎症 / プロスタグランジン合成酵素 / 血液脳脊髄液関門 / リポ多糖 / 神経伝達物質 / PGE2 |
|---|
| Research Abstract |
The expression and localization of mPGES-1 and L-PGDS proteins was examined by immunohistochemical analysis. L-PGDS were expressed in leptomeningeal cells. The signals derived from mPGES-1 were detected in leptomeningeal cells and astrocytes. In the inflammatory model of mice, this mPGES-1 signal was strongly detected in brain capillary endothelial cells, which forms the blood-brain barrier (BBB). In this model, the elimination of PGD2, which is involved in the progression of inflammatory responses, across the BBB was attenuated. From these results, the BBB plays a role in the regulation of the physiological function of prostaglandins in the brain.
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