| Project/Area Number |
14571796
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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 |
病態科学系歯学(含放射線系歯学)
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| Research Institution | Kagoshima University |
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Principal Investigator |
SUENAGA Shigeaki Kagoshima University, University Hospital, Faculty of Medicine and Dentistry, Assistant Professor, 医学部・歯学部附属病院, 講師 (00136889)
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| Co-Investigator(Kenkyū-buntansha) |
INDO Hiroko Kagoshima Univ., Graduate School ofMedical & Dental Sciences, Research Associate, 大学院・歯学総合研究科, 助手 (00301391)
TOMITA Kazuo Kagoshima Univ., Graduate School of Medical & Dental Sciences, Research Associate, 大学院・歯学総合研究科, 助手 (60347094)
KAWATOKO Seigo Kagoshima Univ., Graduate School of Medical & Dental Sciences, Research Associate, 大学院・歯学総合研究科, 助手 (40343363)
MAJIMA Hideyuki Kagoshima Univ., Graduate School of Medical & Dental Sciences, Professor, 大学院・歯学総合研究科, 教授 (60165701)
KAWABATA Yoshihiro Kagoshima Univ., University Hospital, Faculty of Medicine and Dentistry, Research Associate, 医学部・歯学部附属病院, 助手 (70274842)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2003: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2002: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Rheumatoid arthritis / Estrogen / Estrogen receptor / Reactive oxygen species / NO / Lipid peroxidation / Apoptosis / iNOS mRNA / NOS mRNA / 慢性リウマチ性関節炎 / 蛍光バイオイメージング法 |
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| Research Abstract |
The aim of this investigation was to hypothesize that 17β-estradiol(estrogen)can modulate the production and activity of reactive oxygen species(ROS), nitric pxide(NO)synthasis, and lipid peroxidation in fibroblast-like synovial cells, and the effects are dependent on the expressions of estrogen receptor alpha(ER-α).
The results showed that the combined treatment of cytokines and estrogen for the high ER-α expressed fibroblasts decreased the intracellular ROS and NO generation, lipid peroxidation production and subsequent prevented apoptotic cell death, although the low expressed ER-α cells did not show the substantial change.The experiments on levels of iNOS mRNA confirmed the NO levels.These results suggest that estrogen plays an important role in protecting cells against cytokine-induced cell death by controlling the generation of NO and ROS and lipid peroxidation.
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