Forsythoside A regulates pulmonary fibrosis by inhibiting endothelial-to-mesenchymal transition and lung fibroblast proliferation via the PTPRB signaling
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View abstract on PubMed
Summary
This summary is machine-generated.Forsythoside A (FA) effectively treats pulmonary fibrosis (PF) by inhibiting lung fibroblast proliferation and endothelial-to-mesenchymal transition (EndMT). This study reveals FA
Area Of Science
- Pharmacology
- Cell Biology
- Pulmonary Medicine
Background
- Pulmonary fibrosis (PF) is a severe lung disease with limited treatment options.
- Forsythoside A (FA), a compound from Forsythia suspensa, shows potential lung-protective effects, but its anti-fibrotic mechanism is unclear.
Purpose Of The Study
- To investigate the underlying mechanism of Forsythoside A (FA) in treating pulmonary fibrosis (PF).
Main Methods
- Established a PF mouse model using bleomycin (BLM) and treated with FA or pirfenidone.
- Assessed lung histopathology, survival rates, and body weight changes.
- Utilized transcriptome analysis, GEO database analysis, ELISA, RT-qPCR, Western blot, and immunofluorescence to identify molecular targets and pathways, including PTPRB, and tested FA's effects on TGF-β1-stimulated cells.
Main Results
- FA improved survival rates and alleviated lung pathology in PF mice.
- FA reduced key fibrotic markers (e.g., CTGF, α-SMA, TGF-β1) and inhibited endothelial-to-mesenchymal transition (EndMT) and fibroblast proliferation.
- Reduced PTPRB expression was observed in PF patients and mice; PTPRB inhibition attenuated FA's therapeutic effects, indicating PTPRB is a key target.
Conclusions
- FA ameliorates PF by inhibiting lung fibroblast proliferation and EndMT.
- Protein tyrosine phosphatase receptor type B (PTPRB) is identified as a potential molecular target for FA's anti-fibrotic effects.
- FA shows promise as a phytochemical treatment for pulmonary fibrosis.
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