Liao W, Florén C H
Department of Internal Medicine, Lund University, Malmö General Hospital, Sweden.
Scand J Clin Lab Invest. 1992 May;52(3):183-8. doi: 10.3109/00365519209088783.
We previously reported that endotoxins inhibit low-density lipoprotein (LDL) uptake and degradation in Hep G2 cells. In the present study, we tried to elucidate which part(s) of the endotoxin molecules contribute(s) to the inhibitory effect of endotoxins on LDL uptake and degradation. The results show that the endotoxin isolated from Salmonella minnesota Re595 (Re mutant), which lacks polysaccharide, had no effect on the uptake and degradation of 125I-labelled LDL in Hep G2 cells. This mutant form also decreased the inhibitory effects of endotoxins which have complete polysaccharides on cellular LDL uptake and degradation. However, the polysaccharide part of endotoxins by itself had no effect on LDL catabolism by the cells. This suggests that both the polysaccharide and the lipid A parts of endotoxins are needed for the inhibitory effects of endotoxins on LDL uptake and degradation.
我们先前报道过内毒素会抑制Hep G2细胞对低密度脂蛋白（LDL）的摄取和降解。在本研究中，我们试图阐明内毒素分子的哪一部分对其抑制LDL摄取和降解的作用有贡献。结果表明，从缺乏多糖的明尼苏达沙门氏菌Re595（Re突变体）中分离出的内毒素，对Hep G2细胞摄取和降解125I标记的LDL没有影响。这种突变形式还降低了具有完整多糖的内毒素对细胞摄取和降解LDL的抑制作用。然而，内毒素的多糖部分本身对细胞的LDL分解代谢没有影响。这表明内毒素的多糖和脂质A部分对于其抑制LDL摄取和降解的作用都是必需的。
