LAUSR

Objective We aimed to explore the underlying mechanism of Tripterygium glycosides (TGs) in treating systemic lupus erythematosus (SLE) through network-pharmacology approach. Methods The protein targets of TGs’ three active ingredients (triptolide, tripterine, and wilforlide) and SLE were identified by database search. Then, the intersection of the two groups was studied. The drug–target network between the active ingredients of TGs and the overlapping genes was constructed, visualized, and analyzed with Cytoscape software. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment were performed to analyze these genes. Finally, we validated our predictions of the potential targets through docking study. Results A total of 55 overlapping genes were discovered. Results suggested that the TGs’ mechanism in SLE treatment was associated with heat shock protein family A member 5, heat shock protein family A member 8, eukaryotic translation elongation factor 1 alpha 1, and so forth with their related 4042 gene network, which regulated ribosome, spliceosome, viral carcinogenesis, Epstein–Barr virus infection signaling, and so forth. Molecular-docking analysis proved that hydrogen bonding was the main form of interaction. Conclusions Our research provided the protein targets affected by TGs in SLE treatment. The key targets (CASP3, MAPK1, HIF1A, and so forth) involving 4042 proteins became the multitarget mechanism of TGs in SLE treatment.