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首页> 外文期刊>Toxicology Research >Activation of NF-kappa B signaling in rare earth neodymium oxide particle-induced acute lung injury
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Activation of NF-kappa B signaling in rare earth neodymium oxide particle-induced acute lung injury

机译:NF-κB信号在稀土氧化钕颗粒诱导的急性肺损伤中的激活

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摘要

Neodymium is widely applied in industrial materials worldwide, and most of the supply is produced in China. However, neodymium oxide dust exposure can cause pronounced lung injury and pneumoconiosis. This study investigated the process of Nd2O3-induced acute lung injury and explored the activation of NF-kappa B by employing an Nd2O3-instilled rat model. H&E staining, total cell number and total protein amount in broncho-alveolar lavage (BAL) fluid revealed that Nd2O3 instillation caused pronounced acute lung injury, which is characterized by the infiltration of inflammatory cells, alveolar septal thickening, fibroblast proliferation and collagen deposition in the lungs of the rats. Meanwhile, immunoblot analysis and EMSA assay indicated that Nd2O3 instillation induced the NF-kappa B signaling pathway. These results suggest that Nd2O3-induced lung acute injury may be regulated by the NF-kappa B signaling pathway. This report could be the first in vivo mechanistic study of pneumoconiosis induced by Nd2O3, providing insights for the development of clinical therapeutic strategies to prevent Nd2O3-induced pneumoconiosis.
机译:钕在全球范围内广泛应用于工业材料,大部分供应是在中国生产的。然而,氧化钕粉尘的暴露会引起明显的肺损伤和尘肺。这项研究调查了Nd2O3诱导的急性肺损伤的过程,并通过使用Nd2O3滴注的大鼠模型探索了NF-κB的激活。 H&E染色,支气管肺泡灌洗(BAL)液中的总细胞数和总蛋白量显示,Nd2O3滴注引起明显的急性肺损伤,其特征是炎症细胞浸润,肺泡间隔增厚,成纤维细胞增殖和胶原沉积。大鼠的肺。同时,免疫印迹分析和EMSA分析表明Nd2O3滴注诱导了NF-κB信号传导途径。这些结果表明,Nd2O3诱导的肺急性损伤可能受NF-κB信号通路的调节。该报告可能是第一个由Nd2O3引起的尘肺病的体内机制研究,为预防Nd2O3引起的尘肺病的临床治疗策略的发展提供了见识。

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