INTRALIPID INFUSION ABOLISHES ABILITY OF HUMAN-SERUM TO CHOLESTEROL-LOAD CULTURED MACROPHAGES
INTRALIPID INFUSION ABOLISHES ABILITY OF HUMAN-SERUM TO CHOLESTEROL-LOAD CULTURED MACROPHAGES
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DOI：
10.1161/01.atv.9.1.67
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发表时间：
1989-01-01
期刊：
影响因子：
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通讯作者：
DECKELBAUM, RJ
中科院分区：
文献类型：
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作者：
AVIRAM, M;WILLIAMS, KJ;DECKELBAUM, RJ
Intraperoid广泛用于静脉内营养，包含磷脂乳剂颗粒和磷脂脂质体。输注后，甘氨酯乳剂颗粒类似乳糜微粒残留物，因此可能是致动脉粥样硬化的。另一方面，静脉输注磷脂脂质体可使实验性动脉粥样硬化消退，并可消除高胆固醇血症兔血浆对胆固醇负荷培养的巨噬细胞泡沫细胞的能力。为了确定Intralidid输注对细胞胆固醇平衡的净效应，将J-774巨噬细胞与在10% Intralidid输注6小时之前、期间和之后获得的人血清一起孵育18小时。与无血清培养基相比，输注前血清使细胞未酯化胆固醇增加76%，胆固醇酯增加78%。相比之下，6小时输注后获得的血清使细胞未酯化胆固醇减少23%，胆固醇酯减少15%。输注结束后18小时获得的血清仍显示胆固醇负荷能力受损。与这些血清样品孵育的小鼠腹腔巨噬细胞表现相似。与输注前血清相比，输注后血清对125 I-低密度脂蛋白和125 I-极低密度脂蛋白的摄取分别抑制了50%和80%，对胆固醇的排出也增加了46%。我们的结论是，人血清的能力，造成胆固醇积累在培养的巨噬细胞被废除的intraperoid的输液。这种作用是通过细胞胆固醇摄取的减少和细胞胆固醇流出的增加来介导的。如果类似的事件发生在动脉壁，Intraperoid输注可能会抑制体内泡沫细胞的形成。
Intralipid is widely used for intravenous alimentation and contains triglyceride-emulsion particles and phospholipid liposomes. After infusion, triglyceride-emulsion particles resemble chylomicron remnants and thus may be atherogenic. On the other hand, intravenous infusion of phospholipid liposomes produces regression of experimental atherosclerosis and abolishes the ability of hypercholesterolemic rabbit plasma to cholesterol-load cultured macrophage foam cells. To determine the net effect of intralipid infusion on cellular cholesterol balance, J-774 macrophages were incubated for 18 hours with human serum obtained before, during, and after a 6-hour infusion of 10% Intralipid. Compared to serum-free medium, pre-infusion serum increased cellular unesterified cholesterol by 76% and cholesteryl ester by 78%. In contrast, serum obtained after the 6-hour infusion reduced cellular unesterified cholesterol by 23% and cholesteryl ester by 15%. Serum obtained 18 hours after the end of the infusion still showed impaired cholesterol-loading ability. Mouse peritoneal macrophages incubated with these serum samples behaved similarly. Compared to pre-infusion serum, postinfusion serum inhibited cellular uptake of 125I-low density lipoprotein and 125I-very low desity lipoprotin by 50% and 80%, respectively, and also enhanced the efflux of cellulr cholesterol by 46%. We conclude that the ability of human serum to cause cholesterol accumulation in cultured macrophages is abolished by an infusion of intralipid. This effect is mediated by a reduction in cholesterol uptake by the cells and by an increase in cell cholesterol efflux. If similar events occur in the arterial wall, Intralipid infusion might inhibit foam cell formation in vivo.