Objective. In recent years, pulmonary fibrosis caused by paraquat poisoning is still concerned. However, no effective drugs have been developed yet to treat paraquat-induced pulmonary fibrosis. The aim of our research is to investigate whether imrecoxib can inhibit paraquat-induced pulmonary fibrosis and its possible mechanism. Methods. Extraction of primary pulmonary fibrosis cells (PPF cells) in vitro by the method of trypsin digestion. RT-qPCR and western blot were employed to measure the transcription level and protein expression of EMT related markers in paraquat-induced A549 cells. MTT, wound-healing, and Transwell experiments were used to verify the effect of imrecoxib on the proliferation, migration, and invasion of PPF and HFL1 cells. Results. Firstly, our results confirmed that paraquat can induce EMT and activate the NF-κB/snail signal pathway in lung epithelial cell A549. Furthermore, experimental results showed that imrecoxib could repress the proliferation, migration, and invasion of PPF and HFL1 cells. Finally, our study found that imrecoxib can inhibit EMT of paraquat-induced A549 cells by the NF-κB/snail signal pathway. Conclusion. Imrecoxib can inhibit EMT of paraquat-induced A549 cells and alleviate paraquat-caused pulmonary fibrosis through the NF-κB/snail signal pathway. Therefore, imrecoxib is a drug worthy of study in the treatment of paraquat-induced pulmonary fibrosis.

中文翻译：

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Imrecoxib 通过 NF-κB/Snail 信号通路抑制百草枯诱导的肺纤维化

客观。近年来，百草枯中毒引起的肺纤维化仍备受关注。然而，尚未开发出有效的药物来治疗百草枯引起的肺纤维化。我们研究的目的是调查伊瑞昔布是否可以抑制百草枯诱导的肺纤维化及其可能的机制。方法。胰蛋白酶消化法体外提取原发性肺纤维化细胞（PPF细胞）。采用 RT-qPCR 和蛋白质印迹法测量百草枯诱导的 A549 细胞中 EMT 相关标志物的转录水平和蛋白质表达。MTT、伤口愈合和Transwell实验用于验证伊瑞昔布对PPF和HFL1细胞增殖、迁移和侵袭的影响。结果. 首先，我们的研究结果证实百草枯可以诱导肺上皮细胞 A549 中的 EMT 并激活 NF- κ B/snail 信号通路。此外，实验结果表明，imrecoxib可以抑制PPF和HFL1细胞的增殖、迁移和侵袭。最后，我们的研究发现，imrecoxib可以通过NF- κB /snail信号通路抑制百草枯诱导的A549细胞的EMT 。结论。艾瑞昔布可通过 NF- κB /snail 信号通路抑制百草枯诱导的 A549 细胞的 EMT，缓解百草枯引起的肺纤维化。因此，艾瑞昔布是治疗百草枯所致肺纤维化的一种值得研究的药物。