Exploration of the Mechanism of Tanre Qing Injection in Treating Acute Respiratory Distress Syndrome through Network Pharmacology, Molecular Docking, and Animal Experiments.

OBJECTIVE

This study aimed to explore the active components and potential mechanism of Tanre Qing Injection (TRQI) in the treatment of Acute Respiratory Distress Syndrome (ARDS) using network pharmacology, molecular docking, and animal experiments.

METHODS

The targets of active ingredients were identified using the TCMSP and Swiss Target Prediction databases. The targets associated with ARDS were obtained from the GeneCards database, Mala card database, and Open Targets Platform. A Protein-protein Interaction network (PPI) was constructed, and the core targets were subjected to Gene Ontology (GO) function annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Finally, molecular docking technology and a mouse model of lipopolysaccharide-induced acute lung injury validated the experimental results.

RESULTS

The results of network pharmacology showed the active components of TRQI in the treatment of ARDS to be baicalin, chenodeoxycholic acid, oroxylin-A, and ursodeoxycholic acid, and the core targets to be TP53, ESR1, AKT1, JUN, and SRC. KEGG analysis showed 181 signaling pathways, primarily including the IL-17 signaling pathway, endocrine resistance, lipid metabolism, and atherosclerosis. Molecular docking results demonstrated that baicalin, chenodeoxycholic acid, oroxylin-A, and ursodeoxycholic acid in TRQI exhibited the strongest affinity for TP53, ESR1, and SRC. Furthermore, the results of animal experiments have indicated TRQI to have a significant inhibitory effect on inflammatory factors TNF-α, IL-1β, and IL-6, and effectively alleviate the pathological damage of ARDS to lung tissue.

CONCLUSION

TRQI may exert its therapeutic effects on ARDS through multiple targets and pathways, providing a research basis for its clinical application and further development.