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Ophiopogonin D attenuates PM2.5-induced inflammation via suppressing the AMPK/NF-κB pathway in mouse pulmonary
Ying Wang1,2, Dan Li1, Lei Song1
1Department of Respiratory Medicine, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China.
Abstract:
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.
Insights
Ophiopogonin D (OP-D) reduces inflammation caused by fine particulate matter (PM2.5) by activating AMPK and inhibiting the NF-κB pathway. This suggests OP-D is a potential treatment for PM2.5-induced airway inflammation.
Area of Science:
- Environmental Health
- Pharmacology
- Cell Biology
Background:
- Fine particulate matter (PM2.5) exposure causes lung inflammation and systemic injury.
- Ophiopogonin D (OP-D) exhibits known anti-inflammatory properties.
- The protective mechanisms of OP-D against PM2.5-induced inflammation require elucidation.
Purpose of the Study:
- To investigate the anti-inflammatory effects of OP-D on PM2.5-induced acute airway inflammation.
- To explore the underlying molecular mechanisms involving AMPK and NF-κB signaling pathways.
Main Methods:
- Cell viability assays (Cell Counting Kit-8) were performed on mouse lung epithelial (MLE-12) cells.
- Pro-inflammatory cytokine levels (IL-1β, IL-6, IL-8, TNF-α) were measured using ELISA.
- Protein expression and localization (NF-κBp65, p-NF-κBp65, AMPK, p-AMPK) were analyzed via immunofluorescence and western blotting.
- AMPK involvement was assessed using the inhibitor Compound C (CC).
Main Results:
- OP-D significantly reduced PM2.5-induced release of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8).
- OP-D inhibited the nuclear translocation of NF-κBp65 in MLE-12 cells.
- OP-D upregulated AMPK activity and prevented PM2.5-induced NF-κBp65 phosphorylation.
- The anti-inflammatory effects of OP-D were diminished by the AMPK inhibitor CC.
Conclusions:
- OP-D demonstrates significant anti-inflammatory activity against PM2.5-induced airway inflammation.
- The mechanism involves activation of the AMPK pathway and downregulation of the NF-κB signaling pathway.
- OP-D shows potential as a therapeutic candidate for treating PM2.5-related respiratory conditions.
