ロシグリタゾンは,実験的な大動脈動脈瘤の発生と破裂を減少させます
Alun Jones1, Rajdeep Deb, Evelyn Torsney
1Vascular Surgery Research Unit, Cranmer Terrace, Tooting, London, SW17 ORE, UK.
Circulation
|June 10, 2009
まとめ
ロシグリタゾン治療はマウスモデルにおける大動脈動脈瘤の膨張と破裂を著しく減少させた. この保護効果は,炎症媒介体およびアンジオテンシンII受容体の発現の低下と関連していた.
科学分野:
- 心血管研究 循環器科の研究
- 薬理学 薬理学とは
- 動脈硬化症の研究 動脈硬化症の研究
背景:
- 大動脈動脈瘤は,炎症を含む複雑な生物学的プロセスを伴う.
- PPAR-ガンマアゴニストであるロシグリタゾンは,様々なインビボ効果を発揮する.
- この研究では,動脈瘤の発症を予防するロシグリタゾンの有効性を調査した.
研究 の 目的:
- ロシグリタゾンが大動脈動脈瘤の膨張と破裂に及ぼす効果を評価する.
- ロシグリタゾンをアンジオテンシンII誘発性高コレステロール血症マウスモデルで試験する.
主な方法:
- アポリポプロテインE欠乏症のマウスは,アンジオテンシンIIを注入した.
- ロシグリタゾンは,アンジオテンシンII輸注の前と後に投与されました.
- 大動脈の大きさが測定され,28日目に分子分析が行われました.
主要な成果:
- ロシグリタゾンは致命的な大動脈破裂を著しく抑制し,大動脈の膨張を減少させた.
- 血糖,コレステロール,体重,動脈硬化症の有意な差は認められなかった.
- ロシグリタゾンの前治療は,アンジオテンシンII受容体1a型,Eセレクチン,TNF-α,IL-6の発現を低下させた.
結論:
- ロシグリタゾンの投与前後にマウスモデルでは大動脈の膨張と破裂を減少させました.
- 病変の減少は,炎症媒介体発現の減少と相関していた.
- ロシグリタゾンの作用の根本的なメカニズムを完全に解明するには,さらなる研究が必要です.
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