Oyster hydrolysate attenuates osteoarthritis progression by modulating inflammatory signaling and extracellular...

Osteoarthritis (OA) is a chronic degenerative joint disease characterized by progressive cartilage destruction and persistent low-grade inflammation, in which extracellular matrix (ECM) homeostasis plays a pivotal role. Although oyster hydrolysate (OH), derived from Crassostrea gigas (Magallana gigas), is rich in bioactive peptides and has antioxidant and anti-inflammatory properties, its effects on the pathogenesis of OA have not yet been studied. This study aimed to investigate the anti-inflammatory and chondroprotective effects of OH using in vitro and in vivo OA models.

To evaluate the protective effects of OH against OA-associated inflammation and ECM degradation, an in vitro inflammatory model was established by stimulating human chondrosarcoma SW1353 cells with interleukin (IL)-1β, followed by assessment of inflammatory and ECM-related proteins. In vivo, OA was induced by intra-articular injection of monosodium iodoacetate (MIA) into the knee joints of Sprague-Dawley rats, and arthritis-related histological, molecular, and biochemical biomarkers were analyzed in joint tissues and serum.

In vitro, OH reduced IL-1β-induced pro-inflammatory cytokine production and downregulated ECM-degrading enzymes, including a disintegrin and metalloproteinase with thrombospondin motifs-5, matrix metalloproteinase (MMP)-3, and MMP-13, but preserved the expression levels of anabolic proteins, such as aggrecan and collagen II. These effects were associated with the suppression of phosphoinositide 3-kinase/protein kinase B, c-Jun N-terminal kinase, p38, and nuclear factor κB cells signaling pathways. Consistently, oral administration of OH for 14 days alleviated joint swelling, preserved proteoglycan content, and improved the histological Osteoarthritis Research Society International scores in MIA-induced OA rats. OH treatment also reduced the cartilage expression levels of inflammatory cytokines and MMPs and serum levels of IL-1β, IL-6, leukotriene B4, MMP-9, C-reactive protein, and cartilage oligomeric matrix protein.

Overall, our results suggest that OH attenuates OA progression by modulating inflammatory signaling and restoring ECM homeostasis, highlighting its potential as a marine-derived candidate for OA prevention and therapy.