ArticleJournal of inflammation research2026
Deciphering the Potential Mechanism of Cordycepin in Alleviating Ulcerative Colitis via the AKT1 Signaling Pathway: An Integrated Approach Combining Network Pharmacology, Molecular Docking, and Experimental Validation.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Aim: Given the limited availability of safe and effective treatments for inflammatory bowel disease (IBD), we applied an integrated network pharmacology approach to systematically map the targets and pathways of cordycepin, a bioactive compound from Methods: Cordycepin was administered intraperitoneally during dextran sulfate sodium (DSS) exposure in mice, with efficacy evaluated by the disease activity index (DAI) and histopathological analysis. Network pharmacology analysis (TCMSP, CTD, SEA, BATMAN-TCM, GeneCards, and PharmMapper), molecular docking, and molecular dynamics (MD) simulations were performed to identify and validate potential core targets. AKT1 and tight junction protein ZO-1 expression in colonic tissues was assessed by immunohistochemistry (IHC). The involvement of AKT signaling in cordycepin's effects on tight junction integrity and mitochondrial function was further investigated in lipopolysaccharide (LPS)-treated Caco-2 cells using the AKT inhibitor MK2206. Results: Cordycepin (50 mg/kg) significantly attenuated body weight loss and DAI elevation in DSS-treated mice. A total of 361 putative cordycepin-related targets were identified from six public databases, while 2, 072 UC-related targets were obtained from GeneCards, OMIM, and DisGeNET. A total of 199 overlapping targets were functionally enriched in processes including "TNF signaling pathway", "PI3K-AKT signaling pathway" and "cellular response to lipopolysaccharide". The PPI network identified 8 core targets, among which AKT1, NFKB1, RELA and TP53 demonstrated strong binding affinity (binding free energy<-6.0 kcal/mol) with cordycepin in molecular docking and were enriched within the PI3K/AKT pathway. IHC analysis showed that cordycepin reversed alterations of colonic AKT1 and ZO-1 levels in DSS mice. In Caco-2 cells, AKT inhibition with MK2206 attenuated the protective effects on tight junction integrity and mitochondrial function against LPS-induced injury. Conclusion: These findings suggest that prophylactic administration of cordycepin, a promising natural compound, alleviates experimental colitis, potentially through modulation of the PI3K/AKT1 signaling pathway and restoration of epithelial barrier integrity.
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