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Mechanisms of cell uptake, inflammatory potential and protein corona effects with gold nanoparticles

机译:金纳米粒子的细胞摄取,炎症潜能和蛋白质电晕效应的机制

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Aim: To assess inflammation, cellular uptake and endocytic mechanisms of gold nanoparticles (AuNP) in human epidermal keratinocytes with and without a protein corona. Materials & methods: Human epidermal keratinocytes were exposed to 40 and 80 nm AuNP with lipoic acid, polyethylene glycol (PEG) and branched polyethyleneimine (BPEI) coatings with and without a protein corona up to 48 h. Inhibitors were selected to characterize endocytosis. Results & conclusion: BPEI-AuNP showed the greatest uptake, while PEG-AuNP had the least. Protein coronas decreased uptake and affected their mechanism. AuNP uptake was energy-dependent, except for 40 nm lipoic-AuNP. Most AuNP were internalized by clathrin and lipid raft-mediated endocytosis, except for 40 nm PEG was by raftoncaveolae mediated endocytosis. Coronas inhibited caveolae-mediated-endocytosis with lipoic acid and BPEI-AuNP and altered 40 nm PEG-AuNP from raftoncaveolae to clathrin. Inflammatory responses decreased with a plasma corona. Results suggest protein coronas significantly affect cellular uptake and inflammatory responses of AuNP.
机译:目的:评估具有或不具有蛋白质电晕的人表皮角质形成细胞中金纳米颗粒(AuNP)的炎症,细胞摄取和内吞机制。材料与方法:将人类表皮角质形成细胞分别暴露于40 nm和80 nm AuNP上,分别带有硫辛酸,聚乙二醇(PEG)和带有或不带有蛋白质电晕的分支聚乙烯亚胺(BPEI)涂层,时间长达48小时。选择抑制剂以表征胞吞作用。结果与结论:BPEI-AuNP摄取最大,而PEG-AuNP摄取最少。蛋白质电晕会减少摄取并影响其机制。除了40 nm硫辛-AuNP之外,AuNP的吸收是能量依赖的。大部分AuNP都通过网格蛋白和脂质筏介导的内吞作用而被内在化,除了40 nm PEG是通过筏/非小窝介导的内吞作用而被内化的。电晕通过硫辛酸和BPEI-AuNP抑制小窝介导的内吞作用,并将40 nm PEG-AuNP从木筏/无小孔改变为网格蛋白。血浆电晕使炎症反应降低。结果表明,蛋白质电晕显着影响细胞吸收和AuNP的炎症反应。

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