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Advanced Glycation in macrophages induces intracellular accumulation of 7-ketocholesterol and total sterols by decreasing the expression of ABCA-1 and ABCG-1

机译:巨噬细胞中的高级糖基化通过降低ABCA-1和ABCG-1的表达诱导7-酮胆固醇和总固醇的细胞内积累

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摘要

BackgroundAdvanced glycation end products (AGE) alter lipid metabolism and reduce the macrophage expression of ABCA-1 and ABCG-1 which impairs the reverse cholesterol transport, a system that drives cholesterol from arterial wall macrophages to the liver, allowing its excretion into the bile and feces. Oxysterols favors lipid homeostasis in macrophages and drive the reverse cholesterol transport, although the accumulation of 7-ketocholesterol, 7alpha- hydroxycholesterol and 7beta- hydroxycholesterol is related to atherogenesis and cell death. We evaluated the effect of glycolaldehyde treatment (GAD; oxoaldehyde that induces a fast formation of intracellular AGE) in macrophages overloaded with oxidized LDL and incubated with HDL alone or HDL plus LXR agonist (T0901317) in: 1) the intracellular content of oxysterols and total sterols and 2) the contents of ABCA-1 and ABCG-1.
机译:背景技术先进的糖基化终产物(AGE)会改变脂质代谢并降低ABCA-1和ABCG-1的巨噬细胞表达,从而损害胆固醇的逆向转运,该系统将胆固醇从动脉壁巨噬细胞驱动到肝脏,从而将其排泄到胆汁中。屎。氧固醇有利于巨噬细胞的脂质稳态,并驱动胆固醇的逆向转运,尽管7-酮胆固醇,7α-羟基胆固醇和7β-羟基胆固醇的积累与动脉粥样硬化和细胞死亡有关。我们评估了乙醇醛处理(GAD;可引起细胞内AGE迅速形成的乙醛)对巨噬细胞的氧化LDL超负荷作用,并与单独的HDL或HDL加LXR激动剂(T0901317)一起孵育的效果:1)细胞内氧固醇含量和总含量固醇和2)ABCA-1和ABCG-1的含量。

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