This study aimed to explore the effects of atractylodin (ATR) on lipopolysaccharide (LPS)-induced inflammatory response in human airway epithelial cells. The cytotoxicity was assessed by CCK-8 assay. The mRNA expression and concentration of interleukin (IL)-6, IL-8, and mucin 5AC (MUC5AC) were measured by qRT-PCR and ELISA, respectively. Western blotting was performed to determine protein expression. We found that LPS stimulation increased the mRNA expression and concentrations of IL-6, IL-8, and MUC5AC, as well as the expression of Col-I and FN in 16HBE cells, but this effect of LPS was attenuated by ATR treatment. Mechanistically, ATR suppressed LPS-induced activation of the NF-κB pathway in 16HBE cells. Moreover, ATR repressed ovalbumin-induced airway inflammation and NF-kB pathway in mice. In conclusion, ATR attenuated the expression of MUC5AC and ECM in LPS-induced airway inflammation by inhibiting the NF-κB pathway.

中文翻译：

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白术素通过抑制 NF-κB 通路减弱脂多糖诱导的气道炎症中 MUC5AC 和细胞外基质的表达

本研究旨在探讨苍术素（ATR）对脂多糖（LPS）诱导的人气道上皮细胞炎症反应的影响。通过CCK-8测定评估细胞毒性。分别通过 qRT-PCR 和 ELISA 测量白细胞介素 (IL)-6、IL-8 和粘蛋白 5AC (MUC5AC) 的 mRNA 表达和浓度。进行蛋白质印迹以确定蛋白质表达。我们发现 LPS 刺激增加了 16HBE 细胞中 IL-6、IL-8 和 MUC5AC 的 mRNA 表达和浓度，以及 Col-I 和 FN 的表达，但 ATR 处理减弱了 LPS 的这种作用。从机制上讲，ATR 抑制了 LPS 诱导的 16HBE 细胞中 NF-κB 通路的激活。此外，ATR 抑制小鼠卵清蛋白诱导的气道炎症和 NF-kB 通路。综上所述，