Ectoine Inhibits IL-1β-Induced Inflammation by Suppressing the NF-κB Pathway in Chondrocytes and Alleviates Osteoarthritis in a Rat Model

Le résumé fourni par la source

Background: Osteoarthritis (OA) is a degenerative joint disease characterized by inflammation and cartilage destruction, partly mediated by interleukin (IL)-1β-induced nucle factor (NF)-κB activation. Ectoine (Ec) is a natural osmoprotectant with anti-inflammatory properties; however, its effects on NF-κB signaling in OA remain unclear. This study investigated whether ectoine attenuates IL-1β-induced inflammation in chondrocytes by suppressing NF-κB activation and mitigates OA progression in a rat model. Methods: Primary rat chondrocytes were pretreated with ectoine (0–3.0% w/v) and then stimulated with IL-1β (10 ng/mL). Cell viability was evaluated. RT-qPCR and Western blotting were used to determine the expression of inflammatory markers (inducible nitric oxide synthase [iNOS], cyclooxygenase [COX]-2, tumor necrosis factor [TNF]-α, and matrix metalloproteinase [MMP]-3/13), and NF-κB pathway activity was assessed through p65 phosphorylation and inhibitor of NF-κB alpha (IκBα) degradation. In vivo, OA was induced using the modified Hulth method, followed by intra-articular injection of ectoine alone or combined with hyaluronic acid (HA). Cartilage integrity was assessed using Osteoarthritis Research Society International (OARSI) scoring at 8 weeks. Results: Ectoine at 1.5% significantly inhibited IL-1β-induced NF-κB activation, reducing p65 phosphorylation by 59% and IκBα degradation by 41%. This inhibition decreased proinflammatory mediators (iNOS 43%, COX-2 35%, TNF-α 41%) and matrix-degrading enzymes (MMP-3 23%, MMP-13 31%), while increasing type II collagen by 84%. In vivo, ectoine reduced cartilage erosion (OARSI score: 7.0 vs. 10.2 in OA group). The Ec–HA combination improved cartilage retention by 43% compared with ectoine alone. Conclusions: These preclinical findings suggest that ectoine was associated with reduced NF-κB activation markers and attenuated OA-like changes in rat models. The enhanced effect observed with HA supports further investigation of combined therapeutic strategies for OA management.

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.