酸化したリポプロテインは,内皮の表面層を劣化させる: 血小板-内皮細胞結合への影響
H Vink1, A A Constantinescu, J A Spaan
1Department of Medical Physics, University of Amsterdam, Amsterdam, The Netherlands. h.vink@amc.uva.nl
Circulation
|April 4, 2000
まとめ
酸化低密度リポタンパク質 (Ox-LDL) は,内皮の表面層を破壊し,血管壁の粘着性を高めます. この効果は,酸素由来のフリーラジカルによって媒介され,抗酸化物質によって阻害されることがあります.
科学分野:
- 心血管生物学 心血管生物学
- 内皮機能の機能について
- 動脈硬化症の研究研究
背景:
- 内皮表面層 (ESL) は,流れる血液細胞と内皮細胞表面 (EC) の間の分離を維持します.
- 酸化低密度リポタンパク質 (Ox-LDL) は,アテロゲネシスに関与しています.
- ESL障害と血管粘着性におけるOx-LDLの役割は明らかにする必要があります.
研究 の 目的:
- Ox-LDLがESLを破壊し,血管壁の粘着性を高めるとの仮説を検証する.
- Ox-LDLによって引き起こされるESLの変化における,酸素由来のフリーラジカルの役割を決定する.
主な方法:
- 腸内顕微鏡検査は,ハムスターのクレマスター筋肉の赤血球-EC表面距離を観察するために使用されました.
- オックス-LDLは,ネイティブのLDLのCuSO(4) 酸化によって作られました.
- オックス-LDLと抗酸化物質 (スーパーオキシドディスミュータゼとカタラーゼ) がESLの寸法と血小板-EC結合に及ぼす影響を評価した.
主要な成果:
- オックス-LDLは25分以内にESLの次元を60%短縮しました.
- このESLの減少は,血小板-EC結合の一時的な増加と相関していた.
- スーパーオキシドディスミュータゼとカタラーゼの併用投与は,Ox-LDLがESLと血小板粘着に及ぼす効果を完全に阻害しました.
結論:
- 酸素由来のフリーラジカルは,オックス-LDLによる内皮表面層の破壊を媒介する.
- Ox-LDLによるESLの破壊は,血管壁の粘着性を高めるのに寄与する.
- 抗酸化剤の治療は,Ox-LDL誘発のESL変化と関連する血小板粘着を防ぐことができます.
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