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首页> 外文期刊>Nanotoxicology >Monocyte adhesion induced by multi-walled carbon nanotubes and palmitic acid in endothelial cells and alveolar-endothelial co-cultures
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Monocyte adhesion induced by multi-walled carbon nanotubes and palmitic acid in endothelial cells and alveolar-endothelial co-cultures

机译:多壁碳纳米管和棕榈酸在内皮细胞和肺泡-内皮共培养物中诱导单核细胞粘附

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摘要

Free palmitic acid (PA) is a potential pro-atherogenic stimulus that may aggravate particle-mediated cardiovascular health effects. We hypothesized that the presence of PA can aggravate oxidative stress and endothelial activation induced by multi-walled carbon nanotube (MWCNT) exposure in vitro. We investigated the interaction between direct exposure to MWCNTs and PA on THP-1 monocyte adhesion to human umbilical vein endothelial cells (HUVECs), as well as on indirect exposure in an alveolar-endothelial co-culture model with A549 cells and THP-1-derived macrophages exposed in inserts and the effect measured in the lower chamber on HUVECs and THP-1 cells. The exposure to MWCNTs, including a short (NM400) and long (NM402) type of entangled fibers, was associated with elevated levels of reactive oxygen species as well as a decrease in the intracellular glutathione concentration in HUVEC and A549 monocultures. Both effects were found to be independent of the presence of PA. MWCNT exposure significantly increased THP-1 monocyte adhesion to HUVECs, and co-exposure to PA aggravated the NM400-mediated adhesion but decreased the NM402-mediated adhesion. For the co-cultures, the exposure of A549 cells did not promote THP-1 adhesion to HUVECs in the lower chamber. When THP-1 macrophages were present on the cell culture inserts, there was a modest increase in the adhesion and an increase in interleukin-6 and interleukin-8 levels in the lower chamber whereas no tumor necrosis factor was detected. Overall, this study showed that direct exposure of HUVECs to MWCNTs was associated with oxidative stress and monocyte adhesion and the presence of PA increased the adhesion when exposed to NM400.
机译:游离棕榈酸(PA)是潜在的促动脉粥样硬化刺激,可能加剧颗粒介导的心血管健康影响。我们假设PA的存在可以加剧氧化应激和体外激活的多壁碳纳米管(MWCNT)暴露诱导的内皮活化。我们研究了直接暴露于MWCNTs和PA对THP-1单核细胞与人脐静脉内皮细胞(HUVECs)的粘附以及在A549细胞与THP-1的肺泡-内皮共培养模型中间接暴露之间的相互作用。衍生的巨噬细胞暴露在插入物中,并在下腔室中测量对HUVEC和THP-1细胞的影响。暴露于MWCNT(包括短(NM400)和长(NM402)类型的缠结纤维)与HUVEC和A549单培养中活性氧水平升高以及细胞内谷胱甘肽浓度降低有关。发现两种作用均与PA的存在无关。 MWCNT暴露显着增加THP-1单核细胞对HUVEC的粘附,并且共同暴露于PA加重了NM400介导的粘附,但降低了NM402介导的粘附。对于共培养,A549细胞的暴露并不促进THP-1粘附于下腔室的HUVEC。当THP-1巨噬细胞存在于细胞培养插入物上时,下腔室的粘附力适度增加,白介素6和白介素8水平升高,而未检测到肿瘤坏死因子。总体而言,这项研究表明,HUVECs直接暴露于MWCNT与氧化应激和单核细胞粘附有关,而PA的存在会增加暴露于NM400时的粘附力。

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