| Project/Area Number |
09670838
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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 |
Pediatrics
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
NAGAKURA Toshikazu Jikei University School of Medicine, Assosiate Professor, 小児科, 助教授 (30125025)
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| Co-Investigator(Kenkyū-buntansha) |
OBATA Toru Jikei University School of Medicine, Lecturer, DNA医学研究所・分子細胞生物学, 講師 (80119776)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1998: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | cultured human / PGP_2 / EPA / COX-2 / cyfulcine / プロスタグランディンD2 / サイクロオキシケナーゼ2 / ω-3多価不飽和脂肪酸 / PGD2 / COX-2 |
|---|
| Research Abstract |
We have investigated the role of EPA on on PGD2 generation in the cultured human mast cells with IgE-anti-IgE challenge incubation. Although EPA incubation did not affect histamine release from cultured human mast cells in response to challenge, it did decrease PGD2 generation by the inhibiting COX-2 pathway. In contrast, in the cell free homogenate of cultured human mast cells, EPA inhibited both COX-1 and COX-2 activities.
Preincubation with EPA primarily affects the COX-2 pathway in cultured human mast cells and reduces PGD2 generation in response to IgE-anti-IgE challenge incubation. These findings suggest that COX-1 and COX-2 have different substrate flow systems in mast cells. Rhey also suggest that endogenous EPA diet supplemetation would reduce PGD2 production and could serve as an inflammatory substrate in human mast cells.
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