The application of network pharmacology and molecular docking to investigate the mechanisms underlying the therapeutic effects of Salidroside in acute lung injury, along with validation through animal experiments

Objective This study aims to explore the Main targets and potential mechanisms by which Salidroside exerts therapeutic effects on acute lung injury through network pharmacology and in vivo exper imental validation. Methods Potential targets associated with Sal and ALI were identified using the ChEMBL, Super-PRED, Swiss TargetPrediction、Genecards, OMIM, and TTD databases. Overlapping targets were imported into the STRING database to establish a protein-protein interaction network. We conducted comprehensive analyses of GO and KEGG pathways for these overlapping genes utilizing the DAVID database. We selected three that are most relevant to ALI-TNF, SRC, and GAPDH for molecular docking studies. Subsequently, an ALI model was established in Sprague Dawley rats via intraperitoneal injection of lipopolysaccharide, validating the potential mechanism by which Sal treats ALI. Results We identified 327 potential targets associated with Sal's treatment of ALI. Additionally, at the animal level, Compared with the LPS group, secretion levels of IL-6, TNF-α ,and ROS significantly decreased in the Sal group indicating alleviation of lung injury. Conclusion Through network pharmacology combined with experimental validation methods we have determined that Sal can effectively treat ALI by reducing inflammatory factor expression while modulating TNF signaling pathways.