Introduction Ulcerative colitis (UC) is a chronic and progressive inflammatory disease of the intestines, marked by recurrent inflammation along the digestive tract, leading to symptoms such as bloody diarrhea and weight loss, severely impacting patients quality of life. Despite extensive research, current therapeutic treatment for UC still faces challenges in long-term efficacy and safety. Lanatoside C (LanC), as a type of cardiac glycosides, has shown promising anti-inflammatory effects. This study employs network pharmacology to investigate the effects and mechanisms of LanC in the treatment of UC.Method LanC- and UC-associated target genes datasets were retrieved from the Genecards, DisGeNET, and Gene Expre... More
Introduction Ulcerative colitis (UC) is a chronic and progressive inflammatory disease of the intestines, marked by recurrent inflammation along the digestive tract, leading to symptoms such as bloody diarrhea and weight loss, severely impacting patients quality of life. Despite extensive research, current therapeutic treatment for UC still faces challenges in long-term efficacy and safety. Lanatoside C (LanC), as a type of cardiac glycosides, has shown promising anti-inflammatory effects. This study employs network pharmacology to investigate the effects and mechanisms of LanC in the treatment of UC.Method LanC- and UC-associated target genes datasets were retrieved from the Genecards, DisGeNET, and Gene Expression Omnibus database. Integration analysis identified a common set of potential LanC targets for UC treatment. Analyses of Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were performed on these target genes. Additionally, a protein-protein interaction (PPI) network was constructed to identify the top targets with the highest connectivity. Molecular docking and cellular experiments were subsequently carried out to further validated these findings.Results 23 intersecting genes were identified as potential targets of LanC in UC. Among these, KDR, STAT3, ABCB1, CYP3A5, and CYP2B6 emerged as the top 5 targets with high therapeutic potential. Pathway analysis indicated the involvement of fatty acid and lipid metabolism, as well as xenobiotic metabolism pathways, which could be crucial for LanC s efficacy in treating UC. Molecular docking simulations revealed favorable binding interaction between LanC and KDR, STAT3, ABCB1, CYP3A5, and CYP2B6. Furthermore, In vitro experiments demonstrated that LanC significantly inhibits LPS-induced pro-inflammatory cytokines expression in RAW264.7 cells.Conclusion This study demonstrates a comprehensive overview of the therapeutic potential of LanC in UC and elucidates its mechanisms of action. These findings offer a theoretical basis for further optimizing UC clinical therapy and underscore the potential of LanC as a novel therapeutic option for UC.
