摘要
抗磷脂抗体(aPL)是一组异质性自身抗体,β2糖蛋白Ⅰ(β2-GP Ⅰ)和氧化低密度脂蛋白(oxLDL)复合物是导致动脉粥样硬化的自身抗原。抗磷脂抗体能抑制芳香烷基磷酸酯酶(PON)活性,降低总抗氧化能力(TAC),并Fcγ受体介导单核巨噬细胞摄入oxLDL而促进动脉硬化的进程。本文就aPL在动脉粥样硬化发生过程中的作用和分子基础进行综述。
Antiphospholipid antibodies (aPL) are a series of heterogenous autoimmune antibodies. Oxidized low density lipoprotein (oxLDL) complexes with β2-glycoprotein Ⅰ (β2-GP Ⅰ) is thought to be an atherogenic antigen. Antiphospholipid antibodies can reduce total antioxidant capacity ( TAC ) by inhibiting the activity of paraoxonase (PON) , and also can accelerate the progress of atherosclerosis by directing monocyte and macrophage uptake to oxLDL through the Fcγ receptor. In this paper the role and the molecular base of antiphospholipid antibodies in atherosclerosis are reviewed.
出处
《上海第二医科大学学报》
CSCD
2004年第5期397-400,共4页
Acta Universitatis Medicinalis Secondae Shanghai