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目的 研究脂蛋白 (a) [lipoprotein(a) ,Lp(a) ]对巨噬细胞清道夫受体A(scavengerreceptorclassAtypeIandtypeII,ScR A)的影响。方法 利用细胞培养、受体摄取配体及Northern印迹杂交方法 ,观察Lp(a)对从人类单核细胞株细胞形成的巨噬细胞受体摄取乙酰化LDL (acetylatedLDL ,Ac LDL)以及对THP 1细胞形成的巨噬细胞ScR AmRNA表达的影响。结果 人类单核细胞株细胞形成的巨噬细胞对Ac LDL的结合量随Lp(a)浓度的增加而增加 ,而天然LDL对此无影响。加入 5 0μg/mlLp(a) ,巨噬细胞对Ac LDL结合量为 ( 188 0 6± 16 80 )ng/mg蛋白 ,与对照组的 ( 4 8 2 6± 5 61)ng/mg蛋白比较显著增加 (P <0 0 1) ;巨噬细胞对Ac LDL的摄入量为 ( 3 63 80± 11 77)ng/mg蛋白 ,与对照组的 ( 2 2 8 15± 17 0 7)ng/mg蛋白比较显著增加 (P <0 0 5 ) ;巨噬细胞对Ac LDL的降解量为( 94 8 17± 3 1 43 )ng/mg蛋白与对照组的 ( 60 8 68± 3 8 11)ng/mg蛋白比较显著增加 (P <0 0 5 )。加入5 0 μg/mlLp(a) ,其ScR AmRNA表达明显增强 ,与对照组比较增强 4 3 5 6%。 结论 Lp(a)可增强从THP 1细胞形成的巨噬细胞ScR A基因的表达 ,Lp(a)的这种作用可能参与了动脉粥样硬化形成和发展的病理过程。
Objective To investigate the effects of lipoprotein (a) and Lp (a) on scavenger receptor class A type I and type II (ScR A) in macrophages. Methods The effects of Lp (a) on acetylated LDL (acetylated LDL, AcLDL) uptake into macrophages of human monocytic cells were observed by cell culture, receptor uptake ligand and Northern blotting. Effect of ScR AmRNA Expression on Cell-Formed Macrophages. Results The binding of AcLDL to macrophages of human monocytic cells increased with the increase of Lp (a), but no effect was observed with native LDL. The amount of Ac LDL binding to macrophages was (188 0 6 ± 16 80) ng / mg protein with 50 μg / ml Lp (a), which was significantly higher than that of the control group (4826 ± 5 61) ng / mg protein (P <0.01). The macrophage uptake of Ac LDL was (3 63 80 ± 11 77) ng / mg protein, which was significantly higher than that of control group (2 28 15 ± 17 0 7) ng / mg (P <0 05). The degradation of Ac LDL by macrophages was (94 8 17 ± 3 1 43) ng / mg protein compared with that of the control group (60 8 68 ± 3 8 11) ng / mg protein increased significantly (P <0 05). After adding 50 μg / ml Lp (a), the expression of ScR AmRNA increased obviously, which was 43 65% more than the control group. Conclusion Lp (a) can enhance the expression of ScR A gene in macrophages formed from THP 1 cells. This effect of Lp (a) may be involved in the pathological process of atherosclerosis formation and development.