Methylophiopogonanone a attenuates pulmonary fibrosis by inhibiting SPP1-mediated macrophage polarization via the PI3K/Akt pathway - PubMed
3 days ago
- #macrophage polarization
- #pulmonary fibrosis
- #PI3K/Akt pathway
- Methylophiopogonanone A (MOA) attenuates pulmonary fibrosis by targeting SPP1-mediated macrophage polarization via the PI3K/Akt pathway.
- MOA, derived from Ophiopogon japonicus, shows anti-inflammatory and antioxidant properties, with potential antifibrotic effects.
- Study used a bleomycin-induced pulmonary fibrosis mouse model and RAW 264.7 cells to evaluate MOA's efficacy.
- MOA significantly reduced lung fibrosis, improved lung function, and showed no hepatorenal toxicity.
- SPP1 was identified as a key target through transcriptomic and bioinformatics analyses.
- Molecular docking and MST assays confirmed MOA's binding affinity with SPP1.
- MOA inhibited both M1 and M2 macrophage polarization in vivo and in vitro.
- Mechanism involves suppression of SPP1-mediated macrophage polarization via PI3K/Akt pathway inhibition.
- MOA is a promising natural compound for treating pulmonary fibrosis.