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Single-walled carbon nanotubes can induce pulmonary injury in mouse model

机译:单壁碳纳米管可在小鼠模型中诱发肺损伤

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摘要

Carbon nanotubes are a nanomaterial that is extensively used in industry. The potential health risk of chronic carbon nanotubes exposure has been raised as of great public concern. In the present study, we have demonstrated that intratracheal instillation of 0.5 mg of single-walled carbon nanotubes (SWCNT) into male ICR mice (8 weeks old) induced alveolar macrophage activation, various chronic inflammatory responses, and severe pulmonary granuloma formation. We then used Affymetrix microarrays to investigate the molecular effects on the macrophages when exposed to SWCNT. A biological pathway analysis, a literature survey, and experimental validation suggest that the uptake of SWCNT into the macrophages is able to activate various transcription factors such as nuclear factor kappa B (NF-kappa B) and activator protein 1 (AP-1), and this leads to oxidative stress, the release of proinflammatory cytokines, the recruitment of leukocytes, the induction of protective and antiapoptotic gene expression, and the activation of T cells. The resulting innate and adaptive immune responses may explain the chronic pulmonary inflammation and granuloma formation in vivo caused by SWCNT.
机译:碳纳米管是一种广泛用于工业的纳米材料。引起公众极大关注的是,长期暴露于碳纳米管对健康的潜在风险。在本研究中,我们证明了将0.5 mg单壁碳纳米管(SWCNT)气管内滴入雄性ICR小鼠(8周大)可引起肺泡巨噬细胞活化,各种慢性炎症反应以及严重的肺肉芽肿形成。然后,我们使用Affymetrix微阵列研究了暴露于SWCNT时对巨噬细胞的分子效应。生物学途径分析,文献调查和实验验证表明,SWCNT被巨噬细胞摄取能够激活各种转录因子,例如核因子κB(NF-κB)和激活蛋白1(AP-1),这会导致氧化应激,促炎细胞因子的释放,白细胞的募集,保护性和抗凋亡基因表达的诱导以及T细胞的活化。所产生的先天性和适应性免疫反应可以解释SWCNT在体内引起的慢性肺部炎症和肉芽肿形成。

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