Network pharmacology analysis reveals the potential mechanisms of Salidroside in multiple organ dysfunction syndrome-associated liver injury

Background: Multiple organ dysfunction syndrome (MODS) is often accompanied by severe liver injury, yet effective therapeutic options remain limited. Salidroside (SAL), a natural compound derived from Rhodiola rosea, has shown protective effects in various pathological conditions. This study aimed to elucidate the potential molecular mechanisms of SAL in MODS-associated liver injury through a network pharmacology approach. Methods: Potential targets of MODS, liver, and SAL were obtained from the GeneCards database, and overlapping targets were identified by Venn analysis. A protein–protein interaction (PPI) network was constructed using the STRING database, and hub targets were screened by topological analysis. Functional annotation was performed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. An integrated “Disease-Site-Drug-Key Target-KEGG Pathway” network was then established to visualize the potential therapeutic mechanisms. Results: Six intersecting targets were identified, forming a PPI network with 15 interactions. GO enrichment indicated involvement in transcriptional regulation, inflammatory response, apoptosis, and autophagy. KEGG analysis revealed 57 significantly enriched pathways, particularly those related to immune checkpoints, hypoxia-inducible factor 1 (HIF-1) signaling, cancer-associated pathways, lipid metabolism, infectious diseases, and neurodegeneration. The integrative network highlighted the association between SAL, key targets, and multiple signaling pathways relevant to MODS-associated liver injury. Conclusion: This study suggests that SAL may exert protective effects on MODS-related liver injury by modulating inflammation, apoptosis, metabolism, and immune responses. These findings provide a theoretical basis for further experimental validation and potential clinical application of SAL in MODS therapy.