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首页> 外文会议>The 3rd International Conference on Bioinformatics and Biomedical Engineering(iCBBE 2009)(第三届生物信息与生物医学工程国际会议）论文集 >Potential roles of ROS and NF-κB in TNF-α release in rat alveolar macrophages exposed to single-walled carbon nanotubes
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Potential roles of ROS and NF-κB in TNF-α release in rat alveolar macrophages exposed to single-walled carbon nanotubes

机译：ROS和NF-κB在暴露于单壁碳纳米管的大鼠肺泡巨噬细胞中TNF-α释放中的潜在作用

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The pulmonary toxicology of carbon nanotubes (CNTs) was highlighted recently when single-walled carbon nanotubes (SWCNTs) were reported to be highly toxic and fibrotic in mice and in rats when administered by intratracheal instillation. Therefore, it is necessary to evaluate the effects of SWCNTs on human health and the environment before utilizing them on a large scale. The purpose of this study was designed to assess the effects of SWCNTs on tumor necrosis factor-α (TNF-α) release and to elucidate possible molecular mechanisms in primary rat alveolar macrophages as a model system. Our results showed exposure of the cultured alveolar macrophages to SWCNTs elicited a concentration-dependent TNF-α release and reactive oxygen species (ROS) production in alveolar macrophages. In the presence of the antioxidants N-acetyl-Lcysteine (NAC) and glutathione (GSH), the SWCNTs-induced of TNF-α release and ROS production was significantly reduced. SWCNTs treatment caused an activation of the redox-sensitive transcription factor nuclear factor-kappaB (NF-κB). Pretreatment of alveolar macrophages with NF-κB inhibitors, L-1-tosylamido-2-phenylethyl chloromethyl ketone (TPCK) and parthenolide, suppressed SWCNTs-induced TNF-α expression. These results indicate that SWCNTs are able to induce TNF-α release in rat primary alveolar macrophages, at least in part, mediated by oxidative stress and NF-κB activation.
机译：当据报道当通过气管内滴注给药时，单壁碳纳米管（SWCNT）在小鼠和大鼠中具有高毒性和纤维化性时，碳纳米管（CNTs）的肺部毒理学得到了强调。因此，在大规模使用SWCNT之前，有必要评估其对人体健康和环境的影响。本研究的目的是评估SWCNT对肿瘤坏死因子-α（TNF-α）释放的影响，并阐明作为模型系统的原代大鼠肺泡巨噬细胞的可能分子机制。我们的结果表明，将培养的肺泡巨噬细胞暴露于SWCNTs会引起肺泡巨噬细胞中浓度依赖性的TNF-α释放和活性氧（ROS）的产生。在存在抗氧化剂N-乙酰基-L胱氨酸（NAC）和谷胱甘肽（GSH）的情况下，SWCNTs诱导的TNF-α释放和ROS产生显着减少。 SWCNTs处理引起氧化还原敏感的转录因子核因子-κB（NF-κB）的激活。用NF-κB抑制剂，L-1-甲苯磺酰-2-苯基乙基氯甲基酮（TPCK）和小白菊内酯预处理肺泡巨噬细胞可抑制SWCNTs诱导的TNF-α表达。这些结果表明SWCNT能够诱导大鼠原发性肺泡巨噬细胞中TNF-α的释放，至少部分是由氧化应激和NF-κB活化介导的。

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