ArticleAnimal models and experimental medicine2026
Methylophiopogonanone a attenuates pulmonary fibrosis by inhibiting SPP1-mediated macrophage polarization via the PI3K/Akt pathway.
Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Identification and validation of SPP1 as a prognostic biomarker in interstitial lung disease subtypes by single-cell sequencing.Respiratory research · 2026Article
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11 authors.
Funding
Abstract
backgroundIdiopathic pulmonary fibrosis (IPF) is an irreversible, fatal lung disease. Methylophiopogonanone A (MOA), derived from the Chinese medicinal herb Ophiopogon japonicus, has been shown to exhibit anti-inflammatory and antioxidant properties. However, the effects of MOA on pulmonary fibrosis remain unclear. This study aims to evaluate the antifibrotic effect of MOA.
methodsThe antifibrotic efficacy of MOA was evaluated in a bleomycin (BLM)-induced pulmonary fibrosis mouse model, using pirfenidone (PFD) as a positive control. Assessments included histopathology, micro-computed tomography (micro-CT), lung function tests, and serum biochemistry. In vitro, RAW 264.7 murine monocyte/macrophage cells were stimulated with BLM, lipopolysaccharide (LPS), interleukin 4 (IL-4), recombinant secreted phosphoprotein 1 (SPP1) protein, or Spp1 overexpression (OE-spp1) and treated with MOA, PFD, spp1 shRNA (sh-spp1), or the PI3K inhibitor LY294002. Transcriptomics, molecular docking, microscale thermophoresis (MST), immunohistochemistry, immunofluorescence, and Western blot were used for mechanistic exploration.
resultsMOA administration significantly attenuated BLM-induced lung fibrosis and collagen deposition, improved lung function, and did not induce hepatorenal toxicity. Integrated transcriptomic and bioinformatics analyses identified SPP1 as a key potential target. Molecular docking simulation and MST assays further confirmed a favorable binding affinity between SPP1 and MOA. MOA potently inhibited both M1 and M2 macrophage polarization in vivo and in vitro. Mechanistically, MOA attenuated BLM-induced pulmonary fibrosis by suppressing SPP1-mediated macrophage polarization via inhibition of the PI3K/Akt pathway.
conclusionsThis study identifies that MOA is a promising natural compound that alleviates pulmonary fibrosis by inhibiting SPP1-mediated macrophage polarization via the PI3K/Akt pathway.
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