Yokoyama M, Hirata K, Miyake R, Akita H, Ishikawa Y, Fukuzaki H
First Department of Internal Medicine, Kobe University School of Medicine, Japan.
Biochem Biophys Res Commun. 1990 Apr 16;168(1):301-8. doi: 10.1016/0006-291x(90)91708-z.
Endothelial cells are known to play an important role in the regulation of vascular tone. Here we demonstrate that modified low density lipoprotein (LDL) with copper oxidation or phospholipase A2 treatment elicits a potent inhibitory action on endothelium-dependent relaxations evoked by acetylcholine, although native LDL does not affect endothelium-dependent relaxations. Phosphatidylcholine of native LDL is converted to lysophosphatidylcholine during these modifications. Furthermore, lysophosphatidylcholine fraction separated from oxidized LDL (0.5mg.protein/ml) by thin layer chromatography abolished endothelium-dependent relaxations, although the remaining lipid fraction had little effects on endothelium-dependent relaxations. These results indicate that lysophosphatidylcholine is the principal substance for the impairment of endothelium-dependent relaxations by oxidized LDL and phospholipase A2 treated LDL.
已知内皮细胞在血管张力调节中发挥重要作用。在此我们证明,经铜氧化或磷脂酶A2处理的修饰低密度脂蛋白(LDL)对乙酰胆碱诱发的内皮依赖性舒张具有强大的抑制作用,而天然LDL并不影响内皮依赖性舒张。在这些修饰过程中,天然LDL的磷脂酰胆碱会转化为溶血磷脂酰胆碱。此外,通过薄层色谱法从氧化LDL(0.5mg·蛋白/ml)中分离出的溶血磷脂酰胆碱组分消除了内皮依赖性舒张,而其余脂质组分对内皮依赖性舒张几乎没有影响。这些结果表明,溶血磷脂酰胆碱是氧化LDL和磷脂酶A2处理的LDL损害内皮依赖性舒张的主要物质。