ArticleFrontiers in pharmacology2026
Isoviolanthin suppresses IL-1β-induced inflammatory and catabolic responses in chondrocytes.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Knee osteoarthritis (KOA) is characterized by the progressive degeneration of articular cartilage, necessitating novel therapeutic strategies to halt disease progression. Isoviolanthin, a natural flavonoid glycoside, has an unclear mechanism of action in KOA. Methods: We employed network pharmacology and molecular docking, supported by Results: Network pharmacology identified 141 overlapping targets. KEGG enrichment analysis revealed the PI3K-AKT and MAPK signaling pathways as among the most significantly enriched. Molecular docking indicated that isoviolanthin exhibits favorable binding affinities to core targets, including AKT1, MAPK1, and EGFR. In IL-1β-stimulated rat chondrocytes, 25 μM isoviolanthin significantly reduced the expression of inflammatory mediators (CXCL3, CXCL6, IL-6, iNOS, TNF-α, IL-1β, COX2) and promoted the anabolism of extracellular matrix components (collagen II, ACAN, SOX9). The treatment also suppressed matrix-degrading enzymes (MMP3, MMP9, MMP13) and attenuated the IL-1β-induced phosphorylation of PI3K-AKT and MAPK family members. Furthermore, isoviolanthin reversed the IL-1β-induced alterations in RXFP1 expression at both the mRNA and protein levels. Conclusion: These findings demonstrate that isoviolanthin exerts anti-inflammatory and ECM-protective effects in IL-1β-stimulated chondrocytes, likely by inhibiting PI3K-AKT and MAPK signaling and modulating RXFP1 expression. Further validation in human cells and
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