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Exploring the Effect and Mechanism of DaYuan Yin Against Acute Lung Injury by Network Pharmacology, Molecular Docking, and Experimental Validation

Lei Zhang,Wei Zhu,Cong Zhang

Background DaYuan Yin (DYY), a traditional Chinese medicine for lung diseases, requires further study to understand how it improves acute lung injury (ALI). This study seeks to elucidate the material basis and molecular mechanisms underlying the treatment of ALI with DYY through network pharmacology, molecular docking, and experimental validation.Methods DYY’s active components and targets were identified using TCMSP and UHPLC-MS/MS, and a herb-component-target network was created with Cytoscape 3.7.2. ALI target genes were sourced from GeneCards, DisGeNET, and DrugBank. A PPI network was built, with core targets analyzed through GO and KEGG enrichment via Metscape. The therapeutic effects and mechanisms of DYY on LPS-induced ALI in rats were explored, and molecular docking evaluated the interactions between Nrf2, HO-1, TLR4, and the components.Results The study identified 95 active compounds, 234 therapeutic targets, and 2529 ALI-related genes, with 111 shared targets between DYY and ALI. KEGG analysis indicates that the PI3K-AKT, MAPK, and oxidative stress pathways are associated with DYY’s anti-ALI effects. Network pharmacology and UHPLC-MS/MS analysis revealed active ingredients like quercetin, Magnolol, and Wogonin. Compared with the model group, DYY reduced the lung dry–wet ratio (W/D) of ALI rats from (5.31 ± 0.51) to (4.47 ± 0.73)(P < 0.05). Meanwhile, the contents of IL-6 and TNF-α in bronchoalveolar lavage fluid (BALF) and MDA, NO and ROS in lung tissue were also significantly decreased. Notably, DYY enhances UCP2 mRNA expression, boosts Nrf2 and HO-1 expression, and inhibits TLR4-mediated pro-inflammatory mediators. Molecular docking analysis showed that the main components of DYY had strong binding ability with HO-1.Conclusion DYY can alleviate inflammation, oxidative stress, and ALI-related changes by targeting the Nrf2/HO-1 mediated TLR4 pathway, providing insights for developing effective ALI treatments.