Additionally, the TGF-β1/Smad pathway agonist SRI-011381 reversed the inhibitory effects of WYLG on RPF fibrosis, further confirming that WYLG exerts its antifibrotic effect through the TGF-β1/Smad pathway.<h4>Conclusions</h4>WYLG markedly alleviates pulmonary fibrosis both in vivo and in vitro by inhibiting the TGF-β1/Smad signaling pathway and regulating epithelial-to-mesenchymal transition, highlighting its potential as a therapeutic agent for progressive pulmonary fibrosis. Here, TGFB1 is linked to pulmonary fibrosis.