Wedelolactone Attenuates Pulmonary Fibrosis Partly Through Activating AMPK and Regulating Raf-MAPKs Signaling Pathway

The study investigated the effects of Wedelolactone (WEL) on pulmonary fibrosis in mice, finding that WEL attenuated fibrosis by activating AMPK and regulating the Raf-MAPKs signaling pathway. Administering WEL at 10 mg/kg significantly reduced weight loss, pulmonary index, and hydroxyproline content, and decreased pro-inflammatory cytokines IL-1β, TNF-α, and TGF-β1, indicating reduced lung inflammation. Histological analysis showed less severe lung damage and fibrosis. WEL also down-regulated the TGF-β/Smad signaling pathway and inhibited myofibroblast differentiation and epithelial-mesenchymal transition in lung cells. These findings suggested WEL could be a promising therapeutic agent for pulmonary fibrosis, with further research recommended to explore its mechanisms and potential.