ArticleFrontiers in pharmacology2025
Epigallocatechin-3-gallate protects against osteoarthritis-induced chondrocytes dysfunction by regulating PLa2g2a.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Classification, Structure-Activity Relationship, and Anti-Osteoarthritis Mechanism of Natural Flavonoids.Chemistry & biodiversity · 2026Review
- Pomegranate (Veterinary sciences · 2026Review
- From Food Contaminant to Therapeutic Target: Identification of KCNE2 and 5-Azacytidine for Gastric Cancer via Multi-Omics, Machine Learning, and In Vitro Validation.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Article
- Integration of Network Pharmacology, Molecular Docking, and Experimental Validation to Identify the Effect of EGCG on Alleviating Chondrocyte Inflammatory Damage by Targeting ER Stress-STAT3 Crosstalk.Journal of inflammation research · 2025Article
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9 authors.
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Abstract
Background: Osteoarthritis (OA) is a degenerative joint disease characterized by cartilage erosion, subchondral bone remodeling, and synovial inflammation. OA progression is driven by an imbalance between anabolic and catabolic activities in the cartilage extracellular matrix (ECM). Identifying molecular targets involved in chondrocyte (responsible for ECM homeostasis in OA) dysfunction is therefore essential for developing effective OA treatments. Notably, epigallocatechin-3-gallate (EGCG), a polyphenolic compound derived from green tea, is a known pan-assay interference compound (PAINS), which may produce non-specific Methods: We investigated the effects of epigallocatechin-3-gallate (EGCG), a polyphenolic compound derived from green tea, on OA-induced dysfunction in chondrocytes. Primary chondrocytes, extracted from the knee joints of rats and constructed an OA model via IL-1β stimulation, observed cell viability and morphology upon EGCG treatment. Transcriptomic analysis was conducted to screen for differentially expressed genes. Subsequently, an OA model in rats was induced by intra-articular injection of monoiodoacetic acid (MIA), and EGCG was administered for OA treatment to validate the expression of the differentially expressed genes. Results: EGCG could reduce reactive oxygen species (ROS) levels and decreased the expression of inflammatory cytokines IL-β, MMP13, and TNF-α. Transcriptome analysis identified differentially expressed genes, and network pharmacology pinpointed Pla2g2a as a key target of EGCG. Molecular docking studies confirmed a strong binding affinity between EGCG and Pla2g2a. OA model demonstrated that EGCG treatment significantly promoted cartilage repair and increased Pla2g2a expression. Conclusion: These findings underscore the therapeutic potential of EGCG in OA management via antioxidative, anti-inflammatory properties, and Pla2g2a-mediated modulation. Notably, the consistency across
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