高密度リポタンパク質は,C反応性タンパク質の炎症を誘発する活動を中和する

Carol Wadham¹, Nathaniel Albanese, Jane Roberts

¹Division of Human Immunology, Hanson Institute, Institute of Medical and Veterinary Science, Adelaide, South Australia, Australia.

Circulation

|April 14, 2004

まとめ

高密度リポプロテイン (HDL) は,酸化フォスホリピドを通じて内皮細胞に対する炎症促進効果を中和することによって,C反応性タンパク質 (CRP) 誘発の炎症を予防します.

科学分野:

心血管生物学心血管生物学
炎症の研究炎症の研究
脂質代謝についてです.

背景:

C-反応性タンパク質 (CRP) は動脈硬化症のマーカーであり,直接的な炎症促進効果があると示唆されています.
CRPの効果を中和する自然な要因が仮説化されているが,特定されていない.
CRPは,内皮細胞の炎症性粘着分子を誘発する.

研究の目的:

高密度脂質タンパク質 (HDL) がCRP誘発の炎症に及ぼす潜在的な抑制効果を調査する.
HDLがCRPの炎症促進作用に対抗するメカニズムを解明する.

主な方法:

ヒト静脈内皮細胞 (HUVECs) の炎症性粘着分子のCRP誘発アップレギュレーションを評価した.
CRP誘発粘着分子発現に対するネイティブHDLおよび再構成HDL (rHDL) の抑制効果を評価した.
HDL内の活性成分を特定し,抑制効果に責任を負いました.

主要な成果:

CRPは,HUVECにおけるタンパク質とmRNAの両方のレベルでの炎症性粘着分子を著しく上調した.
HDLは,ネイティブと再構成の両方,完全に抑制されたCRP誘発的粘着分子発現.
再構成されたHDL (rHDL) はネイティブHDLよりも100倍強力で,酸化されたリンパ脂は主要な活性成分として特定されました.

結論:

HDLは,内皮細胞内の炎症性粘着分子のCRP誘発のアップレギュレーションを効果的に防ぐ.
抑制メカニズムは,HDLの酸化されたフォスフォリピド成分を含む.
HDLは,動脈硬化症におけるCRP誘発性炎症を緩和するための潜在的な治療目標です.

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