溶血卵磷脂对载脂蛋白E基因缺陷小鼠腹腔巨噬细胞源泡沫细胞胆固醇外流的影响

Effects of Lysophosphatidylcholine on Cholesterol Efflux from Apolipoprotein E Gene Deficient Mouse Peritoneal Macrophage-Drived Foam Cells

以载脂蛋白E基因缺陷小鼠腹腔巨噬细胞源泡沫细胞为研究对象 ,观察溶血卵磷脂对泡沫细胞胆固醇外流的影响以及初步探讨其机制。分离正常及载脂蛋白E基因缺陷小鼠腹腔巨噬细胞 ,以乙酰化低密度脂蛋白负载形成巨噬细胞源泡沫细胞 ,分别以溶血卵磷脂及载脂蛋白AI作为诱导物 ,观察其胆固醇外流情况。结果发现 ,溶血卵磷脂能引起正常组小鼠腹腔巨噬细胞源泡沫细胞胆固醇外流 ,且呈剂量效应关系 ,但载脂蛋白E基因缺陷小鼠组未见明显胆固醇外流 ;载脂蛋白AI能引起两组胆固醇外流 ,且外流量显著高于溶血卵磷脂。结果提示 ,溶血卵磷脂能促进巨噬细胞源泡沫细胞胆固醇外流 。

Aim To explore the effects of lysophosphatidylcholine (LPC) on cholesterol efflux from apolipoprotein E (apo E) gene deficient mouse peritoneal macrophage foam cells. Methods Cholesterol efflux induced by LPC and apo AⅠ from macrophage foam cells separated from normal and apo E gene deficient mice (E 0) mouse loaded with acLDL were measured by enzymetic fluorometry assay. Results LPC could promote cholesterol efflux from macrophage foam cells in relation to both dosage and time. When LPC was incubated with E 0 mouse macrophage foam cells, the released free cholesterol mass was significantly lower than that of normal mouse macrophage foam cells. It was also found that cholesterol efflux induced by apo AⅠ normally occurred in E 0 mouse macrophage foam cells. Conclusion LPC could induce cholesterol efflux from macrophage foam cells, which may occur via apo E pathway.