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TiO 2 nanoparticles induce dysfunction and activation of human endothelial cells

机译:TiO 2纳米颗粒诱导人内皮细胞功能障碍和激活

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摘要

Nanoparticles can reach the blood and cause inflammation, suggesting that nanoparticles-endothelial cells interactions may be pathogenically relevant. We evaluated the effect of titanium dioxide nanoparticles (TiO 2) on proliferation, death, and responses related with inflammatory processes such as monocytic adhesion and expression of adhesion molecules (E- and P-selectins, ICAM-1, VCAM-1, and PECAM-1) and with inflammatory molecules (tissue factor, angiotensin-II, VEGF, and oxidized LDL receptor-1) on human umbilical vein endothelial cells (HUVEC). We also evaluated the production of reactive oxygen species, nitric oxide production, and NF-κB pathway activation. Aggregates of TiO 2 of 300 nm or smaller and individual nanoparticles internalized into HUVEC inhibited proliferation strongly and induced apoptotic and necrotic death starting at 5 μg/cm 2. Besides, TiO 2 induced activation of HUVEC through an increase in adhesion and in expression of adhesion molecules and other molecules involved with the inflammatory process. These effects were associated with oxidative stress and NF-κB pathway activation. In conclusion, TiO 2 induced HUVEC activation, inhibition of cell proliferation with increased cell death, and oxidative stress. (Figure Presented).
机译:纳米颗粒可以到达血液并引起炎症,这表明纳米颗粒与内皮细胞的相互作用可能与致病有关。我们评估了二氧化钛纳米颗粒(TiO 2)对增殖,死亡以及与炎症过程相关的反应的影响,这些炎症过程包括单核细胞粘附和粘附分子(E-和P-选择素,ICAM-1,VCAM-1和PECAM)的表达-1),并在人脐静脉内皮细胞(HUVEC)上带有炎症分子(组织因子,血管紧张素II,VEGF和氧化的LDL受体-1)。我们还评估了活性氧的产生,一氧化氮的产生以及NF-κB途径的活化。 300 nm或更小的TiO 2聚集体和被内化到HUVEC中的单个纳米颗粒从5μg/ cm 2开始强烈抑制增殖并诱导凋亡和坏死性死亡。此外,TiO 2通过增加粘附力和粘附表达诱导HUVEC活化。分子和其他与炎症过程有关的分子。这些作用与氧化应激和NF-κB途径活化有关。总之,TiO 2诱导HUVEC活化,抑制细胞增殖并增加细胞死亡和氧化应激。 (如图所示)。

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