ArticleFrontiers in medicine2025
Multi-targeted inhibition of NF-κB signaling underlies the anti-osteoarthritic effects of BGJXF and its key component dehydrocorydaline.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Insights Into the HIF-1α-Mediated NLRP3 Pyroptosis Pathway in the Regulation of Musculoskeletal Diseases in the High-Altitude Environment.Journal of inflammation research · 2026Review
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7 authors.
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Abstract
Background: Knee osteoarthritis (KOA) poses a significant global health challenge due to its high prevalence and the limited availability of effective treatment options. This study aims to elucidate the multi-target therapeutic mechanisms of bu gan jian xi fang (BGJXF), a traditional Chinese medicine (TCM) formula, in the treatment of KOA. Methods: The study employed integrated liquid chromatography-mass spectrometry (LC-MS) analysis to identify the chemical constituents of BGJXF. Network pharmacology was subsequently utilized to predict potential therapeutic targets shared by BGJXF and KOA. Enrichment analysis was conducted to identify key pathways, while molecular docking was used to assess the binding affinities of principal components to core targets. These mechanisms were further validated through Results: LC-MS analysis identified 91 chemical constituents in BGJXF. Network pharmacology predicted 62 shared therapeutic targets, which were significantly enriched in the AGE-RAGE and HIF-1 signaling pathways. Molecular docking identified dehydrocorydaline as a key component with strong binding affinities to IL-6, BCL2, MMP9, and CCND1. Conclusion: Collectively, these findings indicate that BGJXF, driven by dehydrocorydaline, exerts chondroprotective and anti-inflammatory effects primarily through inhibition of the NF-κB pathway via a multi-target mechanism. The overall therapeutic efficacy of BGJXF may be mediated by its modulation of the dual-pathology axis of "glycometabolic stress-hypoxic injury," which is formed by the AGE-RAGE and HIF-1 signaling pathways. This study lays a pharmacological foundation for the application of BGJXF as a multi-target therapeutic strategy for the management of KOA.
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