Higashihara M, Kinoshita M, Kume S, Teramoto T, Kurokawa K
First Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Biochem Biophys Res Commun. 1991 Dec 31;181(3):1331-6. doi: 10.1016/0006-291x(91)92084-w.
Apolipoprotein E-(apoE-) rich high-density lipoprotein (HDL) of normal subjects showed marked inhibitory effects on platelet aggregation and ATP release as compared with apoE-poor HDL, suggesting that apoE has inhibitory effects on platelet function (Desai et al. J. Lipid Res. 30:831, 1989; Higashihara et al. FEBS Lett. 282:82, 1991). A patient with apoE deficiency showed evidence of decreased platelet aggregability in platelet-rich plasma, but normal aggregability in washed platelets. Both patient's plasma and HDL fraction inhibited platelet aggregation of normal subjects. Patient's HDL reconstituted with recombinant apoE showed further inhibitory effects on platelet function. These results suggest that apoE is a potent, but not unique, inhibitory factor for HDL.
与载脂蛋白E含量低的高密度脂蛋白（HDL）相比，正常受试者富含载脂蛋白E（apoE）的HDL对血小板聚集和ATP释放具有显著的抑制作用，提示apoE对血小板功能具有抑制作用（德赛等人，《脂质研究杂志》30:831，1989；东原等人，《欧洲生物化学学会联合会快报》282:82，1991）。一名apoE缺乏患者的富血小板血浆中血小板聚集性降低，但洗涤血小板的聚集性正常。该患者的血浆和HDL组分均抑制正常受试者的血小板聚集。用重组apoE重构的患者HDL对血小板功能具有进一步的抑制作用。这些结果表明，apoE是HDL的一种强效但非唯一的抑制因子。
