| Project/Area Number |
21591144
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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 |
Metabolomics
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
ARAKI Eiichi 熊本大学, 大学院・生命科学研究部, 教授 (10253733)
KONDO Tatsuya 熊本大学, 大学院・生命科学研究部, 助教 (70398204)
MOTOSHIMA Hiroyuki 熊本大学, 医学部附属病院, 助教 (40398201)
宮村 信博 熊本大学, 大学院・生命科学研究部, 准教授 (40274716)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | エネルギー・糖代謝異常 / 糖尿病大血管合併症 |
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| Research Abstract |
In the present study, we investigated the mechanism(s) of PPARγ activation by inhibiting cPLA_2 on macrophages, and the anti-atherosclerotic effect of cPLA2 inhibition in macrophages and apoE-deficient mice. We revealed that cPLA_2 inhibition induced cyclooxygenase-2 expression and subsequent 15d-PGJ_2 production, resulting PPARγ activation in macrophages. Inhibition of cPLA2 suppressed LPS-induced TNF-α and MCP-1 expression, and induced ABCA1/G1 expression. Moreover, administration of cPLA_2 inhibitor, AACOCF3 suppressed the progression of atherosclerosis in apoE-deficient mice. These results suggest that cPLA2 inhibition has anti-atherosclerotic effects, and cPLA2 may be one of the therapeutic targets for diabetic macrovascular complications.
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