Exploring the mechanism of <i>Rhodiola kirilowii</i> (Regel) Maxim regulating PPARG/PTGS2 to alleviate LPS-induced acute lung injury in mice based on UPLC-Q-TOF-MS ^E combined with system pharmacology

This article investigates how <i>Rhodiola kirilowii</i> (Regel) Maxim (RK) treats acute lung injury (ALI) by analysing its chemical components with UPLC-Q-TOF-MSE. We use databases and software to screen components, identify disease and component targets, create Venn diagrams, map protein-protein interaction networks, conduct GO and KEGG enrichment analyses, and build a "component-target-pathway" network to uncover functional interactions and pathways. Molecular docking was performed using AutoDock Vina to identify the primary active components of RK therapy for ALI and their target sites, followed by visualisation using PyMOL software. A mouse ALI model was developed using LPS injection, confirmed <i>via in vivo</i> experiments. Database screening identified 18 active compounds and 62 potential targets for RK in ALI treatment. Liquiritin showed strong binding to PPARG and PTGS2. Animal experiments indicated that liquiritin improved LPS-induced lung injury and inflammation in ALI mice. RK may alleviate LPS-induced acute lung injury in mice by inhibiting the TLR4/MYD88/NF-κB pathway and regulating PPARG and PTGS2 expression.