【摘要】 观察Ca2 + 在细胞介导的低密度脂蛋白氧化过程中的作用。巨噬细胞分别培养在不加处理因素、添加了2 0mg L低密度脂蛋白以及低密度脂蛋白加不同浓度钙离子拮抗剂维拉帕米 (0 ,2 5 ,5 0 ,10 0 ,15 0 μmol L)的培养基中。测定培养基中的丙二醛、丙二烯、髓过氧化物酶的活性和浓度的变化以及细胞内的髓过氧化物酶的活性及含量的变化。结果显示 ,维拉帕米显著地抑制巨噬细胞介导的低密度脂蛋白的氧化和巨噬细胞髓过氧化物酶的分泌 ,且这种抑制作用呈浓度依赖性。这些结果提示维拉帕米引起钙离子向巨噬细胞膜内转移减少 ,细胞分泌髓过氧化物酶的随之减少 ,髓过氧化物酶氧化修饰低密度脂蛋白下降更多还原

【Abstract】 To investigate the mechanisms involved in oxidative modification of LDL, murine peritoneal macrophages were used to identify the role of Ca 2+ in cell mediated oxidation of LDL. Confluent macrophages were incubated in basal medium alone or in medium containing low density lipoprotein (20mg/L) and verapamil (0,25,50,100,150μmol/L), a calcium channel blocker. Changes of MDA ?dienes?MPO activity and MPO concentration in medium were measured and changes of MPO activity ? MPO concentration in cell were also monitored. Verapamil significantly blocked macrophage-mediated LDL oxidation and secretion of MPO and the inhibition of verapamil was dose-dependent. Verapamil leads to the reduction of transmembrane calcium, that results in reduction of the secretion of MPO by macrophages. Then LDL oxidation decreases because of the reduction of the activity and concentration of MPO in media.更多还原