Higashihara M
First Department of Internal Medicine, Faculty of Medicine, University of Tokyo.
Nihon Rinsho. 1992 Feb;50(2):282-6.
Low-density lipoprotein (LDL) at a concentration of 100 micrograms/mL, which is near the dissociation constant (Kd) of LDL-binding, had a maximal stimulatory effect on agonist-induced platelet aggregation. Anti-LDL receptor monoclonal antibody (C-7), like native LDL, induces a transient increase in intracellular Ca2+ and a shape change of human platelets. On the other hand, high-density lipoprotein (HDL) inhibited platelet function. ApoE-rich HDL, as well as, apoE.DMPC potently inhibited platelet aggregation in a dose-dependent manner. ApoE.DMPC stimulated the release of cholesterol into the supernatant, suggesting that apoE plays a major role in the inhibitory effect of apoE-rich HDL in platelet function, presumably due to the release of cholesterol from the plasma membrane.
浓度为100微克/毫升的低密度脂蛋白（LDL）接近LDL结合的解离常数（Kd），对激动剂诱导的血小板聚集具有最大刺激作用。抗LDL受体单克隆抗体（C-7）与天然LDL一样，可诱导人血小板细胞内Ca2+短暂增加和形态改变。另一方面，高密度脂蛋白（HDL）抑制血小板功能。富含载脂蛋白E的HDL以及载脂蛋白E.二肉豆蔻酰磷脂酰胆碱（apoE.DMPC）以剂量依赖方式有效抑制血小板聚集。载脂蛋白E.二肉豆蔻酰磷脂酰胆碱刺激胆固醇释放到上清液中，表明载脂蛋白E在富含载脂蛋白E的HDL对血小板功能的抑制作用中起主要作用，可能是由于胆固醇从质膜释放。
