The potential targets of salidroside in the treatment of pediatric epilepsy are revealed by network pharmacology, molecular docking, and cell experiments

Salidroside has been reported as a neuroprotective drug in central nervous system diseases, including epilepsy. Herein, this study aimed to explore the potential mechanism of salidroside in pediatric epilepsy (PE). Targets of salidroside or PE were screened using online databases. The intersection targets were obtained through Venny analysis. String was used for analysis of protein-protein interaction network. Associated pathways were enriched by Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analysis. The molecular docking was accomplished by the AutoDock Vina. 75 targets of salidroside were found in PE treatment. Interleukin-1 beta (IL1B), Interleukin-6 (IL6), Protein Kinase Bα 1(AKT1), and Caspase-3 (CASP3) were core therapeutic targets of salidroside for PE. GO and KEGG showed that inflammatory response, lipid, and atherosclerosis were mainly associated pathways. Molecular docking indicated the high binding between salidroside and 4 core targets. Furthermore, salidroside suppressed KA-induced microglia activation and inflammation. Moreover, salidroside treatment could down-regulate the protein expression of IL1B, IL6, AKT1, and CASP3 in KA-induced microglia. Our study found that salidroside might exert the neuroprotective effect by targeting IL1B, IL6, AKT1, or CASP3, providing a new idea for the therapy of for PE.