School of Public Health, Baotou Medical College, Baotou, 014030, Inner Mongolia, PR China.
School of Public Health, Baotou Medical College, Baotou, 014030, Inner Mongolia, PR China.
Ecotoxicol Environ Saf. 2020 Jun 1;195:110455. doi: 10.1016/j.ecoenv.2020.110455. Epub 2020 Mar 18.
Inhalation of neodymium oxide, a type of rare earth metal, can induce various respiratory diseases, such as lung tissue inflammation, but the associated mechanisms underlying this induction are still unclear. In this study, we explored the role and mechanisms of circular RNA in neodymium oxide-induced airway inflammation. Our study showed that treating human bronchial epithelial (16HBE) cells with neodymium oxide caused an inflammatory response by upregulating the expression of interleukin-8 (IL-8) and interleukin-1 beta (IL-1β). Quantitative real-time polymerase chain reaction (qRT-PCR) analyses revealed significant downregulation of circRNA_0000638 in neodymium oxide-treated 16HBE cells. Data from functional analyses further showed that circ_0000638 inhibited inflammation induced by neodymium oxide in 16HBE cells. circ_0000638 targeted miR-498-5p and further increased the expression of NKRF (NF-κB repressing factor), which inhibited the activation of NF-κB (nuclear factor κB). Moreover, circ_0000638 reduced the expression of IL-8 and IL-1β by inhibiting NF-κB activation in neodymium oxide-treated 16HBE cells. These results suggest that circ_0000638 can inhibit NF-κB activation by competitively binding to miR-498-5p, further downregulating the expression of IL-8 and IL-1β in neodymium oxide-treated 16HBE cells.
吸入氧化钕，一种稀土金属，可引起各种呼吸道疾病，如肺部组织炎症，但这种诱导的相关机制尚不清楚。在这项研究中，我们探讨了环状 RNA 在氧化钕诱导的气道炎症中的作用和机制。我们的研究表明，用氧化钕处理人支气管上皮（16HBE）细胞会通过上调白细胞介素-8（IL-8）和白细胞介素-1β（IL-1β）的表达引起炎症反应。定量实时聚合酶链反应（qRT-PCR）分析显示，氧化钕处理的 16HBE 细胞中 circRNA_0000638 的表达明显下调。功能分析的数据进一步表明，circ_0000638 抑制了 16HBE 细胞中氧化钕诱导的炎症。circ_0000638 靶向 miR-498-5p，进一步增加了 NKRF（NF-κB 抑制因子）的表达，从而抑制了 NF-κB（核因子 κB）的激活。此外，circ_0000638 通过抑制 NF-κB 激活，减少了氧化钕处理的 16HBE 细胞中 IL-8 和 IL-1β 的表达。这些结果表明，circ_0000638 可以通过竞争性结合 miR-498-5p 抑制 NF-κB 的激活，从而进一步下调氧化钕处理的 16HBE 细胞中 IL-8 和 IL-1β 的表达。
