Peer-reviewed veterinary case report
An investigation into the efficacy and mechanism of Berchemia kulingensis leaves in suppressing synovial tissue inflammation in a rat model of gouty arthritis.
- Journal:
- Journal of ethnopharmacology
- Year:
- 2026
- Authors:
- Xiong, Youyi et al.
- Affiliation:
- Department of Pharmacy · China
- Species:
- rodent
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: The pharmacological activities of Berchemia kulingensis (BK) leaves, traditionally used as a tea for joint discomfort relief in Chinese folk, remain unexplored. AIM OF THE STUDY: To explore the potential therapeutic effects of BK-leaves on gouty arthritis (GA), thus providing a scientific basis for their folk use and pharmaceutical development. MATERIALS AND METHODS: The secondary metabolites of BK-leaves were analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) technology. Combined with activity prediction, the therapeutic potential and related mechanisms of action were further systematically explored through GA rat models and in vitro cell models. RESULTS: The prediction of the identified compounds' biological activity suggests BK leaves may have potential therapeutic effects on GA. Animal experiments show that extract of BK-leaves alleviated synovial inflammation in rats, reduced the concentrations of tumor necrosis factor (TNF)-α, interleukin-1β (IL-1β), IL-6, IL-8, cyclooxygenase (COX)-2, and matrix metalloproteinase (MMP)-9, inhibited protein expression of NLR family pyrin domain-containing protein 3 (NLRP3) and Toll-like receptor 4 (TLR4), as well as phosphorylation of proteins including p65 subunit of nuclear factor (NF)-κB, NF-κB inhibitor kinase (IKK) alpha/beta, and signal transducer and activator of transcription 3 (STAT3), while simultaneously upregulated protein expression of the nuclear factor κB inhibitor alpha (IκBα) (P < 0.05, P < 0.01, or P < 0.001). Additionally, BK-leaf extract inhibited xanthine oxidase (XO) activity in vitro (P < 0.05, 0.01, or 0.001). CONCLUSION: BK-leaf has potential therapeutic value for GA, and its mechanism may be related to regulating the TLR4-NF-κB signaling pathway and inhibiting XO activity.
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Search related cases →Original publication: https://pubmed.ncbi.nlm.nih.gov/41475180/