Wang S P, Feng Y M, Feng Z C, Wu W S, Wang C B, An C R, Jiang W G
J Tongji Med Univ. 1989;9(1):48-53. doi: 10.1007/BF02933744.
It was demonstrated by using lipoprotein lipase (LPL) inhibitor benzene boronic acid (BBA) that LPL played a major role in the accumulation of triglycerides (TG) in mouse peritoneal macrophages exposed to rabbit normal very low density lipoproteins (N-VLDL). There wwere less free fatty acids (FFA) and much more N-VLDL-TG left in the media containing BBA than in the controls. TG accumulation in the cells was greatly diminished or even prohibited by BBA. Thus, we obtained direct evidence that LPL played a more important role than the receptor did in the uptake of N-VLDL-TG by mouse macrophages. The mechanisms of LPL action were discussed.
通过使用脂蛋白脂肪酶(LPL)抑制剂苯硼酸(BBA)证明,在暴露于兔正常极低密度脂蛋白(N-VLDL)的小鼠腹膜巨噬细胞中,LPL在甘油三酯(TG)积累中起主要作用。与对照组相比,含有BBA的培养基中游离脂肪酸(FFA)较少,剩余的N-VLDL-TG更多。BBA大大减少甚至阻止了细胞内TG的积累。因此,我们获得了直接证据,表明在小鼠巨噬细胞摄取N-VLDL-TG的过程中,LPL比受体发挥了更重要的作用。文中还讨论了LPL的作用机制。