天然属性抗氧化型低密度脂蛋白IgM亚类抗体对动脉粥样硬化形成的机制探讨

Role of natural antiox-LDL subclass IgM antidodies in formation of atherclerosis

目的探讨天然属性抗氧化低密度脂蛋白(oxLDL)IgM亚类抗体在动脉粥样硬化中的作用。方法选取部分小鼠巨噬细胞分为LDL组、铜(Cu)oxLDL组与对照组,LDL组、CuoxLDL组分别预先与LDL、冰CuoxLDL孵育,然后与对照组进行黏附实验。3A6,5G8和2H7分别与^(125)I-CuoxLDL混合,另取部分巨噬细胞分为3A6组,5G8组和2H7组,分别加入上述处理的^(125)I-CuoxLDL进行黏附实验。采用油红O染色以及细胞内脂质分析泡沫细胞。结果 CuoxLDL组结合^(125)I-CuoxLDL水平明显低于对照组和LDL组(P<0.01)。5G8组和2H7组结合^(125)I-CuoxLDL水平与对照组无显著差异(P>0.05),而3A6组结合^(125)I-CuoxLDL水平明显低于对照组、5G8组和2H7组,差异有统计学意义(P<0.01)。油红O染色结果显示,未活化的巨噬细胞未见油滴,3A6组有少量油滴,而对照组油滴明显增加。与对照组相比,3A6组胞内胆固醇酯水平明显降低了45%,且TG水平明显降低170%(P<0.01)。结论抗体3A6能够有效阻断未活化巨噬细胞与ox-LDL相结合,抑制动脉粥样硬化的发生发展。

Objective To study the role of natural antiox-LDL subclass IgM antibodies in formation of atherclerosis.Methods The macrophages from mice were divded into LDL group,Cuox-LDL group and control group.The macrophages in LDL group and Cuox-LDL group were precultured with LDL and Cuox-LDL.Adhesion experiment was performed in control group.3 A6,5 G8 and 2 H7 were incubated.The macrophages were divided into 3 A6 group,5 G8 group and 2 H7 group.Adhesion experiment was performed by adding the pretreated ^（125）I Cuox-LDL.The binding parameters of macrophages and ^（125）I Cuox-LDL in different groups were recorded.Foam cells were analyzed by cell lipid analysis with oil red O staining.Results The bound ^（125）I Cuox-LDL level was significantly lower in Cuox-LDL group than in control group and LDL group（P0.01）.No significant difference was found in bound ^（125）I Cuox-LDL level between 5 G3 group and 2 H7 group（P0.05）.The bound ^（125）I Cuox-LDL level was significantly lower in 3 A6 group than in control group,5 G8 group and 2 H7 group（P0.01）.Oil red O staining showed no oil drop in macrophages,but a small number of oil drops in 3 A6 group and a large number of oil drops in control group.The cholesterol and TG in macrophages reduced 45% and the TG reduced 170%in 3 A6 group,which were significantly lower than those in control group（P0.01）.Conclusion Antiox-LDL IgM subclass antibody 3 A6 can effectively prevent the binding of unactivated macrophages to ox-LDL,reduce the occurrence and progression of atherosclerosis.