Levilactobacillus brevis KU15147 Attenuates MIA-Induced Osteoarthritis by Modulating Inflammatory Responses and Cartilage Metabolism.

This study investigated the protective effects of Levilactobacillus brevis KU15147 on monosodium iodoacetate (MIA)-induced osteoarthritis in rats and inflammatory chondrocyte models. After 10 days of oral administration, osteoarthritis was induced via two intra-articular injections of MIA (50 μl of 60 mg/mL) at 3-day intervals. Experimental groups included normal control (NC), MIA-treated control (C), a positive control treated with indomethacin (PC, 3 mg/kg body weight/day), L. brevis KU15147 low-dose (15147-L, 1 × 108 CFU/rat/day), and L. brevis KU15147 high-dose (15147-H, 1 × 109 CFU/rat/day) groups. Knee thickness measurements, micro-computed tomography, and histological analyses were performed to evaluate joint structural changes. Serum levels of PGE2, LTB4, 5-lipoxgenase, tumor necrosis factor-α, interleukin (IL)-6, and IL-1β were measured, and cartilage metabolism- and inflammation-related gene expression were analyzed via quantitative real-time PCR. Furthermore, H2O2- or lipopolysaccharide (LPS)-stimulated chondrocytes were used to assess cytoprotective and anti-inflammatory effects ex vivo. MIA administration-induced cartilage degeneration, joint swelling, inflammatory mediator elevation, as well as catabolic and pro-inflammatory gene expression upregulation. L. brevis KU15147 treatment attenuated structural damage, suppressed systemic and local inflammatory responses, and restored the balance between anabolic and catabolic gene expression in both in vivo and ex vivo models. These findings suggest that L. brevis KU15147 exerts protective effects against osteoarthritis progression through the modulation of inflammatory pathways and cartilage metabolism.