摘要
目的 :观察氧化低密度脂蛋白 (OxLDL)及其成分溶血卵磷脂 (LPC)对小鼠腹腔巨噬泡沫细胞胆固醇外流的影响及其机制的初步探讨。方法 :( 1)以载脂蛋白AI(apoAI)分别诱导OxLDL和乙酰化低密度脂蛋白 (AcLDL)负载小鼠腹腔巨噬细胞所形成的巨噬泡沫细胞 ,观察其胆固醇外流情况。 ( 2 )分离正常及apoE基因缺陷 (E0 )小鼠腹腔巨噬细胞 ,以AcLDL负载形成巨噬泡沫细胞 ,分别以LPC及apoAI作为诱导物 ,观察其胆固醇外流情况。结果 :( 1)apoAI能引起AcLDL组巨噬泡沫细胞胆固醇大量外流 ,而OxLDL组外流明显受阻。 ( 2 )LPC能引起正常组小鼠腹腔巨噬泡沫细胞胆固醇外流 ,且呈剂量效应关系 ,但E0 组未见明显外流 ;apoAI能引起两组的胆固醇外流 ,且外流量显著高于LPC。结论 :( 1)OxLDL能造成胆固醇外流途径受阻。 ( 2 )LPC能促进巨噬泡沫细胞胆固醇外流 。
AIM: To explore the effects of oxidized low density lipoprotein (OxLDL) and one of its component— lysophosphatidylcholine (LPC) on cholesterol efflux from mouse macrophage foam cells. METHODS: (1) Cholesterol efflux induced by apoAI from mouse peritoneal macrophage foam cells loaded with OxLDL or acylated LDL(AcLDL) was measured. (2) Cholesterol efflux induced by LPC and apoAI from macrophage foam cells separated from normal or apoE gene deficient (E 0) mouse loaded with AcLDL were measured. RESULTS: (1) When the macrophage foam cells were incubated with apoAI, cholesterol efflux from AcLDL-induced macrophage foam cells increased significantly compared to that of OxLDL-induced macrophage foam cells. (2) LPC promoted 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 cholesterol mass was significantly lower than that of normal mouse macrophage foam cells. It was also found that cholesterol efflux induced by apoAI normally occurred in E 0 mouse macrophage foam cells. CONCLUSIONS: (1) OxLDL accumulated cholesterol in macrophages and impair cholesterol efflux. (2) LPC induced cholesterol efflux from macrophage foam cells, which may occur via apoE pathway.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2003年第9期1246-1249,共4页
Chinese Journal of Pathophysiology
基金
广东省自然科学基金资助项目 (No .990 0 90 )
中华医学基金会 (CMB)资助项目