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<p>Osteoarthritis (OA) is a chronic joint disease characterized by cartilage degeneration, synovial inflammation and imbalanced subchondral bone remodeling, in which chronic inflammation plays a critical role. This study aimed to investigate the potential molecular mechanism of magnoflorine against OA and verify it via in vitro experiments. Potential targets of magnoflorine were predicted using TCMSP, SwissTargetPrediction and OA-related databases, followed by intersection gene and functional enrichment analyses via STRING and Cytoscape. Molecular docking revealed strong binding affinity of magnoflorine with IL-1β, TNF-α and MMP-9. KEGG analysis indicated that magnoflorine mainly modulated TNF, MAPK and NF-κB signaling pathways. In IL-1β-stimulated MC3T3-E1, RAW264.7 and mouse primary chondrocytes, magnoflorine (25–100&#xa0;μg/mL) showed no obvious cytotoxicity and restored cell viability. It promoted osteogenic migration and mineralization, upregulated osteogenic markers, and inhibited RANKL-induced osteoclastogenesis. Mechanistically, magnoflorine suppressed abnormal activation of the p38 MAPK/NF-κB pathway and promoted SRC/STAT3 phosphorylation, thus downregulating pro-inflammatory and matrix-degrading factors while upregulating IL-10. In chondrocytes, it upregulated Col2a1 and downregulated MMP3/MMP13. In summary, magnoflorine mitigates OA progression by enhancing osteoblast function, inhibiting osteoclastogenesis, maintaining cartilage homeostasis and attenuating inflammation via blocking the NF-κB/MAPK pathway, suggesting its potential as a candidate agent for OA treatment.</p>

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Exploration of the therapeutic potential of magnoflorine against osteoarthritis progression using network pharmacology and in vitro validation

  • 期刊论文

  • 发表日期：

    2026年3月17日

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  • Chengbin Wang,
  • Lu Cui,
  • Mengxiao Tantai,
  • Gangning Feng,
  • Zhe Cai,
  • Yu Feng

摘要

Osteoarthritis (OA) is a chronic joint disease characterized by cartilage degeneration, synovial inflammation and imbalanced subchondral bone remodeling, in which chronic inflammation plays a critical role. This study aimed to investigate the potential molecular mechanism of magnoflorine against OA and verify it via in vitro experiments. Potential targets of magnoflorine were predicted using TCMSP, SwissTargetPrediction and OA-related databases, followed by intersection gene and functional enrichment analyses via STRING and Cytoscape. Molecular docking revealed strong binding affinity of magnoflorine with IL-1β, TNF-α and MMP-9. KEGG analysis indicated that magnoflorine mainly modulated TNF, MAPK and NF-κB signaling pathways. In IL-1β-stimulated MC3T3-E1, RAW264.7 and mouse primary chondrocytes, magnoflorine (25–100 μg/mL) showed no obvious cytotoxicity and restored cell viability. It promoted osteogenic migration and mineralization, upregulated osteogenic markers, and inhibited RANKL-induced osteoclastogenesis. Mechanistically, magnoflorine suppressed abnormal activation of the p38 MAPK/NF-κB pathway and promoted SRC/STAT3 phosphorylation, thus downregulating pro-inflammatory and matrix-degrading factors while upregulating IL-10. In chondrocytes, it upregulated Col2a1 and downregulated MMP3/MMP13. In summary, magnoflorine mitigates OA progression by enhancing osteoblast function, inhibiting osteoclastogenesis, maintaining cartilage homeostasis and attenuating inflammation via blocking the NF-κB/MAPK pathway, suggesting its potential as a candidate agent for OA treatment.