| Project/Area Number |
11671135
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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 | Saitama Medical School |
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Principal Investigator |
INOUE Ikuo Saitama Medical School,, 医学部, 講師 (60232526)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
|
| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | peroxisome proliferator-activated receptor α (PPARα) / peroxisome proliferator-activated receptor γ (PPARγ) / human umbilical vein endothelial cells (HUVEC) / nicotine adenine dinucleotide phosphate (NADPH) oxidase / cyclooxygenase-2 / interleukin-1β / Cu2+, Zn2+-superoxide dismutase (CuZn-SOD) / ベザフェブレート / 核内受容体(PPAR)α / 遺伝子導入 / プロモーター領域 / 酸化ストレス / カタラーゼ / Cu-Zn-SOD |
|---|
| Research Abstract |
We examined the effects of peroxisome proliferator-activated receptor α (PPARα) and PPARγ on the production and expression of inflammatory cytokines and on enzyme expression involving prostaglandin and superoxide production in cultured human umbilical vein endothelial cells (HUVEC). PPARα and PPARγ significantly reduced interleukin-1β and -6 mRNA expression and their protein levels in the culture medium, and also inhibited cyclooxygenase-2 mRNA expression and their protein levels. Moreover, the mRNA levels of p22phox, a 22-kD subunit and the protein levels of p47phox, a 47-kD subunit of nicotine adenine dinucleotide phosphate (NADPH) oxidase, was decreased by induction of PPARα and PPARγ. This unique anti-inflammatory effect in addition to its hypolipidemic action, may be beneficial in preventung the vascular complications that are induced by hyperlipidemia.
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