| Project/Area Number |
13671496
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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 |
Orthopaedic surgery
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| Research Institution | NIIGATA UNIVERSITY |
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Principal Investigator |
OGOSE Akira (2002) NIIGATA UNIVERSITY University Medical Hospital. Lecturer, 医学部附属病院, 講師 (80323963)
羽生 忠正 (2001) 新潟大学, 大学院・医歯学総合研究科, 助教授 (20189591)
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| Co-Investigator(Kenkyū-buntansha) |
YAMADA Toshiyuki Jyuntendo University, Faculty of Medicine, Associate professor, 医学部, 助教授 (50211636)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2001: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | Reactive Amyloidsis / SAA / PPAR α / Fibrate / PPARα |
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| Research Abstract |
This study demonstrated that
1) Fenofibrate inhibited reactive AA-amyloidosis by reducing SAA in an inflammatory murine model.
2) Fenofibric acid inhibited the SAA production from hepatocyte (HepG2 cell) stimulated by pro-inflammatory cytokines such as IL-1β and IL-6.
3) Fenofibric acid inhibited the production of IL-1β and IL-6 from monocyte (RAW264 cell) stimulated by lipopolysaccharide.
4) The PPARα expression was not found in monocyte (macrophage) by RT-PCR. Peroxisome proliferator response element (PPRE), to which the PPARα-RXR heterodimer directly bind, was not found on the gene arrangement of IL-1, IL-6 and SAA.
5) The activation of nuclear factor κB (NF-κB), which regulates transcription of genes encoding inflammatory cytokines and SAA, was down regulated in the inflammatory condition in vitro.
6) Fenofibrate did not inhibit adjuvant arthritis in rat model. The expression of PPARα is not observed in the human synovium of rheumatoid arthritis.
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