Objective: This study aimed to look into the therapeutic potential of rutinoside in reducing articular cartilage degeneration in a rat model of osteoarthritis generated by monosodium iodoacetate (MIA). Methods: We formed three groups of male Wistar rats: the OA, rutinoside, and control groups. Monosodium iodoacetate (3.0 mg) was injected intra-articularly into the knee joint to cause osteoarthritis. For four weeks, oral administration of rutinoside at 100 mg/kg/day was given to the groups that were given the treatment. Histological examination, immunohistochemistry, and biochemical tests were used to assess the level of articular cartilage injury, oxidative damage, catabolic activity, and biomarker expression. Results: The results showed that treatments with rutinoside significantly reduced the damage to articular cartilage in rats with MIA-induced osteoarthritis. Compared to the osteoarthritis group, the rutinoside-treated groups showed enhanced cartilage structure, proteoglycan content, and chondrocyte organization. Immunohistochemistry revealed reduced NFκB, IL-1β, and MMP-13 expressions in the rutinosidetreated groups, indicating suppressed inflammatory and catabolic activity in chondrocytes. Additionally, rutinoside treatment increased SOD activity and decreased MDA levels, which showed less oxidative damage to the joint. A substantial drop in CTX-II levels was found by biochemical research, indicating less type II collagen breakdown. Conclusion: According to a study, rutinoside effectively reduces oxidative damage and catabolic activity in chondrocytes, which can lead to decreased articular cartilage loss in a rat model of MIA-induced osteoarthritis. The study also found that rutinoside can control critical biomarkers such as NFκB, IL-1β, SOD, MDA, MMP-13, and CTX-II, highlighting its potential as a treatment for osteoarthritis. These findings provide valuable insights into using natural chemicals as a promising treatment for OA and suggest that rutinoside could potentially modulate the critical interplay between oxidative stress, inflammation, and chondrocyte catabolism in osteoarthritis. However, further research is required to understand the underlying molecular mechanisms and evaluate rutinoside's translational potential for OA therapy.
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