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サイクロオキシゲネーゼ-2,非対称ディメチルルギニン,および非ステロイド抗炎症薬による心血管の危険性

Emanuela Ricciotti1, Cecilia Castro2, Soon Yew Tang1

  • 1Department of Systems Pharmacology and Translational Therapeutics and the Institute for Translational Medicine and Therapeutics, Perelman School of Medicine, Philadelphia, PA (E.R., S.Y.T., D.M., S.D.R., H.M., X.L., N.F.L., A.M.W., G.A.F.).

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まとめ

非ステロイド性抗炎症薬 (NSAIDs) は,サイクロオキシゲネーゼ2 (COX-2) 抑制によってメチラーギニンを変化させない. メチラーギニンのレベルは,COX-2の影響によるのではなく,腎臓機能が損なわれた場合にのみ上昇する.

キーワード:
エンドセリウム腎臓窒素酸化物薬理学についてプロスタグランディン

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科学分野:

  • 心血管薬学
  • 腎臓生理学
  • メタボロミクス

背景:

  • 非ステロイド性抗炎症薬 (NSAIDs) は,潜在的にサイクロオキシゲナーゼ2 (COX-2) を阻害し,心臓保護性プロスタサイクリンを減少させることで,心血管のリスクを増加させることが知られている.
  • 別の仮説では,NSAIDsは,血管全体に窒素酸化物 (NO) の作用を阻害する腎臓由来メチラーギニンを増加させることで,心臓保護を損なう可能性があることを示唆しています.

研究 の 目的:

  • L-アルギニン/酸化窒素経路に対するCOX-2抑制またはデリエーションの影響を調査する.
  • 骨格関節炎患者のNSAIDの使用がメチラーギニンのレベルに影響するかどうかを判断する.

主な方法:

  • タモキシフェン誘導性COX-2ノックアウトのマウスおよび骨格関節炎患者で標的および非標的代謝効果を活用した.
  • 血と腎臓の代謝体,L-アルギニン/酸化窒素経路の遺伝子発現,選択性COX-2阻害剤 (ロフェコキシブ,セレコキシブ,パレコキシブ) の効果を分析した.
  • アルギニンとメチラーギニンの変化,血圧,腎機能 (血クレアチニン) の評価

主要な成果:

  • マウスにおけるCOX- 2の消去または抑制は,プラズマまたは腎臓のアルギニンおよびメチラーギニン濃度を変えない.
  • 選択的なCOX- 2阻害剤はマウスではメチラーギニンを上昇させなかったし,NSAIDの暴露は骨格関節炎患者にも影響を及ぼさなかった.
  • 血管新生II誘発性高血圧と腎機能低下のマウスでは,血非対称性ジメチルギニンが増加し,腎機能が回復すると正常化する.

結論:

  • プラズマメチラーギニンは,COX- 2の消去または抑制によって影響を受けません.
  • 甲基アルギニンの値上昇は,COX- 2活性と直接に関連していないが,腎不全と関連している.
  • NSAIDによって引き起こされる心血管疾患のメカニズムは,COX-2抑制によるメチラーギニンの増加を含まない場合があります.