Deng Y Z, Feng Z C, Wang H X, Jiang W G, Zhong Y Q, Wang C F
Department of Biochemistry, Tongji Medical University, Wuhan.
J Tongji Med Univ. 1991;11(1):39-44. doi: 10.1007/BF02893186.
Macrophages were incubated with 125I-VLDL for 5 h in presence or absence of lipoprotein lipase (LPL) inhibitor, benzene boronic acid (BBA). Both the uptake and degradation of 125I-VLDL by macrophages were saturable, and the uptake and degradation curves were virtually identical. When macrophages were incubated with 125I-VLDL for 10 h in presence of BBA, the uptake and degradation of 125I-VLDL were still saturable. However, in absence of BBA, the uptake and degradation were no longer saturable. The results suggest that with macrophages incubated with VLDL for a shorter period, VLDL was taken up predominantly via receptor pathway, with a longer period of incubation, LPL played a striking role in uptake of VLDL.
在有或没有脂蛋白脂肪酶(LPL)抑制剂苯硼酸(BBA)存在的情况下,将巨噬细胞与125I-VLDL孵育5小时。巨噬细胞对125I-VLDL的摄取和降解均具有饱和性,且摄取曲线和降解曲线几乎相同。当在BBA存在的情况下将巨噬细胞与125I-VLDL孵育10小时时,125I-VLDL的摄取和降解仍具有饱和性。然而,在没有BBA的情况下,摄取和降解不再具有饱和性。结果表明,巨噬细胞与VLDL孵育较短时间时,VLDL主要通过受体途径被摄取,而孵育时间较长时,LPL在VLDL的摄取中起显著作用。