ArticleACS omega2025
Mechanism of the Proprietary Chinese Medicine "JiuLiWan" to Treat Ulcerative Colitis Revealed by Network Pharmacology, Molecular Docking, and Experimental Verification
Article in ACS omega, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Potential mechanism of Lactiflorin in treating ulcerative colitis via modulation of the PI3K/AKT pathway: a study integrating network analysis, bioinformatics analysis, and experimental evidence.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Ailanthone as a novel AKT1 inhibitor that induces mitochondrial apoptosis and exerts anti-tumor activity in cervical cancer.Translational cancer research · 2026Article
- Flavonoids fromFrontiers in microbiology · 2026Article
- Research Progress on the Biological Activities and Clinical Applications of Pseudoprotodioscin.Current issues in molecular biology · 2025Review
- Quercetagitrin Ameliorates Alzheimer-Like Pathologies Associated with TNFα/NFκB Pathway in APP/PS1 Mice.ACS omega · 2025Article
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Authors and funding
14 authors.
Funding
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Abstract
JiuLiWan (JLW), as a classic traditional Chinese medicine formula, has been clinically used against ulcerative colitis (UC). However, the exact mechanism of its therapeutic effect remains unclear. This study aims to explore and validate the main components and pharmacological mechanism of JLW in the treatment of UC through network pharmacology, molecular docking, and cell experiments. Network pharmacology analyses indicated a total of 107 main components and 286 core targets of JLW against UC. Pathway enrichment analysis demonstrated the involvement of PI3K-AKT, MAPK, Ras, Rap1, TNF, T cell receptor, HIF-1, C-type lectin receptor, VEGF, and Th17 cell differentiation signal pathways in the efficacy of the formula. The molecular docking results indicated that the prominent components (ailanthone (AIL), butylidenephthalide, honokiol, dehydrocostuslactone, ganoderic acid A, atractylenolide I, neokurarinol, glycyrrhetinic acid, palmatine, tangeretin, and bruceine A) could bind to core targets AKT1, P53, STAT3, c-JUN, and ERK1. Subsequently, AIL was used as a representative compound to conduct cell experiments to verify its role and mechanism in anti-inflammation and immunomodulation. Interestingly, AIL could switch Jurkat T cells into a quiescence state without activating the inflammatory and immune status. However, AIL could significantly decrease the levels of interleukin-2 (IL-2) and interferon-gamma (IFN-γ), as well as the expression of surface activation markers CD69 and CD25, in PMA/ionomycin-activated Jurkat T cells by suppressing the RAF/ERK/STAT3 signaling pathway and increasing the phosphorylation of p53. This study combines network pharmacology prediction with experimental verification
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