ArticleJournal of inflammation research2025
Effects of Baicalin on Gout Based on Network Pharmacology, Molecular Docking, and in vitro Experiments.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Dual action of baicalin against renal fibrosis in hyperuricemic nephropathy: targeting PANX1-P2Y6 signaling and gut microbiota dysbiosis.Journal of molecular histology · 2026Article
- Green NiO nanoparticle catalyzed synthesis of novel triazolopyrimidine derivatives with physicochemical characterization and computational evaluation for gout therapy.Scientific reports · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Baicalin is a flavonoid of Scutellaria baicalensis Georgi. It possesses antipyretic, analgesic, and anti-inflammatory effects. It has great potential to treat gout. A network pharmacology approach, molecular docking and experimental validation were applied to investigate the pharmacological mechanisms of baicalin in treating gout. Methods: The potential targets of baicalin were retrieved from the TCMSP, PharmMapper, STITCH, and Swiss Target Prediction databases. The gout-related targets were retrieved from the DrugBank, TTD, and Genecards databases. Then, the potential targets and signaling pathways were acquired via protein-protein interaction (PPI), as well as the Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Subsequently, the key targets were selected to dock with baicalin based on molecular docking. Finally, in vitro experiments were conducted to further validate the predictions. Results: A total of 318 potential targets of baicalin and 752 gout-related targets were screened. TNF, VEGFA, MMP9, PTGS2, and TLR4 might be the hub therapeutic target genes. The TLR4/NF-κB signaling pathway might be the foremost pathway in baicalin against gout. Moreover, molecular docking showed that baicalin combined well with TNF, VEGFA, MMP9, COX-2, and TLR4, respectively. The results of cell experiments suggested that baicalin could reduce the levels of inflammatory cytokines by inhibiting the TLR4/NF-κB signaling pathway in MSU-stimulated THP-1 cells and regulate the expression of these hub targets. Conclusion: These results revealed that baicalin possesses "multitarget, multipathway, multilevel" regulatory effects. From a therapeutic standpoint, baicalin may be a promising anti-inflammatory agent for alleviating gout.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.