• Am. J. Med. Sci. · Jul 2024

    Elucidating the Mechanism of the Tibetan Medicine Sanguotang in Treating Gouty Arthritis through Network Pharmacology and in vivo Experiments.

    • Cairang Nima, Ladan Wanma, Xianghong Jing, Caidan Duojie, Duojie Gazang, and Zengjia Ren.
    • Department of Tibetan Medicine Clinic, Tibetan Medical College of Qinghai University, Xining 810016, PR China; Department of Tibetan Medicine External Treatment, Tibetan Medical Hospital of Qinghai Province, Xining 810007, PR China.
    • Am. J. Med. Sci. 2024 Jul 1; 368 (1): 687968-79.

    BackgroundWe explored the mechanisms of Sanguotang (SGT), a Tibetan medicine, in treating gout arthritis (GA).MethodsThe main active components, action targets, and disease targets of SGT were identified through TCMSP databases. The gene functions were analyzed using protein interaction (PPI) networks, Gene Ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and molecular docking. A GA model induced by monosodium urate was established in rats. The ankle joint swelling was observed. The levels of uric acid (UA) and albumin (ALB) in rat serum were measured. Hematoxylin and eosin (HE) staining was conducted to examine the pathological changes in rat ankle joints.ResultsTwenty-nine active components of SGT with proven efficacy and 66 intersection targets were identified, primarily involved in inflammation and immune regulation pathways. The PPI results revealed that the key targets of SGT against GA included ALB, IL6, TNF, TP53, and PTGS. Molecular docking showed favorable binding energy between the ALB protein and the active components. The results from animal experiments demonstrated that SGT effectively alleviated the inflammatory reaction in ankle joints, and decreased UA and ALB levels. Furthermore, SGT effectively inhibited the proliferation of synovial cells in the ankle joint cavity, prevented infiltration of inflammatory cells, and protected synovial tissue, thereby improving GA.ConclusionsSGT comprehensively contributes to the treatment of GA by regulating UA metabolism, reducing the release of inflammatory factors, and modulating immune and inflammatory pathways.Copyright © 2024 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.

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