Ophiopogonin D attenuates PM2.5‑induced inflammation via suppressing the AMPK/NF‑κB pathway in mouse pulmonary epithelial cells
- Ying Wang
- Dan Li
- Lei Song
- Hui Ding
Affiliations: Department of Respiratory Medicine, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China
- Published online on: October 5, 2020 https://doi.org/10.3892/etm.2020.9268
Copyright: © Wang
et al. This is an open access article distributed under the
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Exposure to fine particulate matter, such as particulate matter of ≤2.5 µm in diameter (PM2.5), causes pulmonary inﬂammation and injury to other organs. It has been reported that Ophiopogonin D (OP‑D) has anti‑inflammatory activity. The aim of the present study was to investigate this anti‑inflammatory activity of OP‑D on PM2.5‑induced acute airway inflammation and its underlying mechanisms. The viability of PM2.5‑treated mouse lung epithelial (MLE‑12) cells with or without OP‑D treatment was determined using a Cell Counting Kit‑8 assay. The corresponding levels of IL‑1β, IL‑6, IL‑8 and TNF‑α were examined via ELISA. Subcellular localization of NF‑κBp65 was detected using immunofluorescence staining. The expression levels of AMP‑activated protein kinase (AMPK), phosphorylated (p)‑AMPK, NF‑κBp65 and p‑NF‑κBp65 were analyzed using western blotting. The selective AMPK inhibitor Compound C (CC) was utilized to investigate the involvement of AMPK in the protection against PM2.5‑induced cell inflammation by OP‑D treatment. The results demonstrated that OP‑D significantly ameliorated the PM2.5‑stimulated release of proinflammatory cytokines (TNF‑α, IL‑1β, IL‑6 and IL‑8) and inhibited the translocation of NF‑κBp65 from the cytoplasm to the nucleus in MLE‑12 cells. Moreover, OP‑D significantly prevented the PM2.5‑triggered phosphorylation of NF‑κBp65 and upregulated AMPK activity. The anti‑inflammatory activity of OP‑D could also be attenuated by the AMPK‑specific inhibitor CC. The present results suggested that the anti‑inflammatory activity of OP‑D was mediated via AMPK activation and NF‑κB signaling pathway downregulation, which ameliorated the expression of proinflammatory cytokines. Therefore, OP‑D could be a candidate drug to treat PM2.5‑induced airway inflammation.