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アスピリンは,ファクターXIII Val34Leuポリモルフィズムによる心臓保護効果を変化させます

Anetta Undas¹, Wojciech J Sydor, Kathleen Brummel

¹Department of Medicine, Jagiellonian University School of Medicine, Cracow, Poland.

|January 8, 2003

まとめ

アスピリンは,Leu34ポリモルフィズムを有する個体において,因子XIII (FXIII) の活性化をより効果的に抑制する. この強化された阻害は,Leu34キャリアは,低用量アスピリンから,より大きな心筋梗塞のリスク低下を得ることを示唆しています.

科学分野:

心血管医学心血管医学
薬剤遺伝学薬剤遺伝学について
ヘモスタシスとトランボシス

背景:

(F) XIII Leu34ポリモルフィズム因子 (F) XIII Leu34の心臓保護機構は完全に理解されていません.
アスピリンのフィブリノゲンおよびトロンビン活性化されたFXIIIに対する効果は,Val34Leuの多形態化との潜在的な相互作用を示唆する.

研究の目的:

アスピリンが,Val34Leu多形態症の個体におけるXIII因子の活性化に差異的に影響するかどうかを調査する.

主な方法:

7日間のアスピリン (75 mg/d) 治療前と後の,Leu34キャリアとVal34同位体におけるFXIII活性化率の比較.
マイクロ血管損傷部位から採取した血のサンプルに定量的なウエスタン・ブロッティングを用いた.

主要な成果:

Leu34アレルは,トロンビン媒介によるFXIII活性化率を著しく増加させた.
アスピリンは,Val34ホモジゴートと比較して,Leu34キャリアにおいてFXIII活性化をより深く抑制した.
トロンビン生成に対するアスピリンの効果は,2つのグループ間で類似していました.

結論:

アスピリンのFXIII活性化の阻害は,Leu34キャリアにおいて強化される.
Leu34キャリアは,低用量アスピリン療法で,より大きな心筋梗塞のリスク低下を経験することがあります.

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