Abstract
Osteoarthritis is a progressive joint disease characterized by the activation of different molecular mediators, including proinflammatory cytokines, reactive oxygen species, metalloproteinases and nociceptive mediators. Anacardium occidentale L. is a medicinal plant with anti-oxidative and anti-inflammatory properties. In this study we evaluate the effects of cashew nuts (from Anacardium occidentale L.) oral administration on an experimental model of painful degenerative joint disease. Monosodium iodoacetate (MIA) was intraarticularly injected, and cashew nuts were orally administered three times per week for 21 days, starting the third day after MIA injection. Nociception was evaluated by a Von Frey filament test, and motor function by walking track analysis at 3, 7, 14 and 21 days after osteoarthritis. Histological and biochemical alteration were examined at the end of the experiment. Cashew nuts administration reduced pain-like behavior and showed antioxidant activities, restoring biochemical serum parameters: glutathione (GSH), catalase (CAT) levels, glutathione peroxidase (GPx) activity and lipid peroxidation. Moreover, cashew nuts ameliorated radiographic and histological alteration, resulting in decreased cartilage degradation, pro-inflammatory cytokines and metalloproteinases levels and mast cells recruitment. Our results demonstrated that the oral assumption of cashew nuts counteracts the inflammatory and oxidative process involved in osteoarthritis.
Highlights
Osteoarthritis is one of the most leading causes of disability
Allodynia is a prominent symptom of osteoarthritis, which represents a debilitating characteristic and is often treatment-resistant
Osteoarthritis was induced by Monosodium iodoacetate (MIA) injection in the knee joint [18]
Summary
Osteoarthritis is one of the most leading causes of disability. Worldwide evaluations show that18% of women and 9.6% of men ≥60 years are affected by osteoarthritis [1]. Osteoarthritis is one of the most leading causes of disability. 18% of women and 9.6% of men ≥60 years are affected by osteoarthritis [1]. It is a complex pathology characterized by an inflammatory mediators storm released by bone, cartilage and synovium [2]. These mediators activate nociceptive and degradative pathways associated with the development of the disease [2,3]. Allodynia is a prominent symptom of osteoarthritis, which represents a debilitating characteristic and is often treatment-resistant. Pathology modification strategies for reversing or arresting the development of joint degeneration have been suggested to impact on pain generation
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