Study on the mechanisms of action of Ephedra sinica Stapf extract in treating acute exacerbation of chronic obstructive pulmonary disease (AECOPD).

This study integrated UPLC-QTOF-MS, network pharmacology and in vitro experiments to explore the therapeutic mechanisms of Ephedra sinica Stapf (ESS) in acute exacerbation of chronic obstructive pulmonary disease (AECOPD). UPLC-QTOF-MS identified 50 compounds in ESS. For network pharmacology analysis, we screened ESS-related and AECOPD-related targets, identifying 288 overlapping targets as their common targets. STRING was used to construct a PPI network, and DAVID for GO/KEGG enrichment analyses. Core PPI proteins included TP53, SCR, STAT3, PIK3CA and PIK3R1, with enriched pathways covering MAPK, TNF and NF-κB signaling. In A549 cells induced by CSE+LPS to establish the AECOPD model, ESS intervention regulated cell viability, promoted apoptosis, and reduced levels of inflammatory cytokines IL-1β, IL-6, and TNF-α. Western blot results confirmed ESS modulated key proteins in the MAPK/NF-κB pathway. Collectively, ESS exerts anti-AECOPD effects possibly by inhibiting inflammation and regulating the MAPK/NF-κB signaling pathway, highlighting its potential as a candidate for AECOPD therapy.