ArticlePloS one2026
Epigallocatechin-3-gallate attenuates PAR-2-mediated inflammatory signaling and preserves markers of mitochondrial integrity in osteoarthritic chondrocytes.
Article in PloS one, 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
Epigallocatechin-3-gallate (EGCG), the principal catechin of green tea, exhibits broad anti-inflammatory properties; however, its effect on protease-activated receptor-2 (PAR-2)-mediated signaling in osteoarthritis (OA) has not been investigated. Here, we report that EGCG (5-10 µM) dose-dependently suppresses PAR-2 expression at both mRNA and protein levels in lipopolysaccharide (LPS)-stimulated human chondrocytes derived from bone marrow mesenchymal stem cells. This upstream inhibition attenuated ERK1/2 phosphorylation (pERK/total ERK ratio reduced below basal levels at 10 µM) and produced concordant suppression of three functionally linked effector arms: (i) pro-inflammatory cytokines (TNF-α, IL-1β, MCP-1), with near-maximal inhibition at 10 µM and a saturation plateau at 20 µM; (ii) the SOX4-ADAMTS-5 catabolic axis (81.9% and 66.2% protein reduction, respectively); and (iii) RANK/RANKL surface expression. EGCG also restored mitochondrial membrane potential and biomass to near-homeostatic levels. Crucially, small interfering RNA (siRNA)-mediated PAR-2 silencing reduced LPS-induced TNF-α by ~38% and substantially blunted EGCG's incremental efficacy, supporting PAR-2 as a predominant, though not exclusive, mediator of EGCG's anti-inflammatory action. The effective concentrations employed are physiologically attainable through dietary green tea consumption, as documented by a comprehensive survey of EGCG content across 36 commercial varieties. These findings support PAR-2 as a candidate upstream target of EGCG in OA chondrocytes and suggest a mechanistic model involving PAR-2 → ERK1/2 → TNF-α/SOX4/ADAMTS-5, through which a dietary polyphenol exerts coordinated anti-inflammatory and anti-catabolic effects, while preserving structural and thermodynamic markers of mitochondrial integrity.
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