载脂蛋白C Ⅲ拮抗低密度脂蛋白对内皮细胞的损伤

The Protective Effect of Apolipoprotein C Ⅲ on Endothelial Cell Injury Induced by Low Density Lipoprotein

为探讨高密度脂蛋白-载脂蛋白和载脂蛋白CⅢ在保护内发细胞免受低密度脂蛋白损伤方面所起的作用。将体外培养的人脐静脉内皮细胞分成对照组、高密度脂蛋白-载脂蛋白+低密度脂蛋自组、载脂蛋白CⅢ+低密度脂蛋白组和低密受脂蛋白组4组。通过观察细胞形态变化、测定乳酸脱氢酶释放率和前列环素合成，来观察低密度脂蛋白对内皮细胞形态和功能的影响、结果发现．低密度脂蛋白可引起内皮细胞收缩、细胞膜损伤、乳酸脱氢酶释放增加和前列环素合成减少。预加入高密度脂蛋白-载脂蛋白或载脂蛋白CⅢ（100mg／L）．内皮细胞再受到低密度脂蛋白（1.5g/L）的损伤时，细胞形态和功能不发生明显改变。提示高密度脂蛋白-载脂蛋白和载脂蛋白CⅢ均能部分拮抗低密度脂蛋白对内皮细胞的损伤。

Aim To investigate the protective effect of apolipoprotein(apo) C Ⅱon the morphology and func- tion of human umbilical vein endcthelial cells,injured by low density lipoprotein (LDL) in vilro. Methods Cultured huynan endothelial cells derived from umbilical vein were divided into four groups:control, high density lipoprotein (HDL)-apo + LDL,apo C Ⅱ+LDL and LDL group. which were observed the morphological changes with phase-contrast and transmission electron microscope and measurcd the re- lease of lacate dehydrogenase (LDH) and level of 6-ke-to-prostaglandin Fla (PGFla).Results Endothelial cells after being injured by LDL showed cell contraction. Increased release of LDH ayld decreased jevel of 6-keto-PGFla. Howev- er, normal morphology and LDH rtlease as well as prostacyclin (PGI2) syntllesis in endothelial cells were found when HDL-apo or apo C Ⅱ was added to culture media before LDL inJury.Conclusious Both HDL-apo and apo C Ⅱ could re-sist the injurious effect of LDL on cultured endothelial cells.