Abstract
In this study was investigated the effect of treatment with a fish oil preparation (FOP) on inflammatory and histopathological parameters in a rat model of adjuvant-induced arthritis (AIA). Paw edema, the severity of secondary lesions, the number of synovial leukocytes, and serum nitric oxide and cytokines concentrations were evaluated. Histological changes in cartilage and bone of the femorotibial articulation in the paws were analyzed by hematoxylin/eosin and sirius red-hematoxylin staining. Oral treatment with the FOP (75, 150, and 300 mg/kg) that was initiated on the day of arthritis induction (day zero) and maintained for 21 days inhibited inflammatory signals and prevented morphological changes in cartilage and bone of the femorotibial articulation of the paws. These effects could be at least partially attributable to inhibitory and modulatory actions of the FOP on the production and release of nitric oxide and cytokines that participate in the pathophysiology of AIA.
Highlights
Fish oil (FO) is a rich source of n-3 long-chain polyunsaturated fatty acids (PUFAs), especially eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3), and has many health benefits
3.1 Treatment with fish oil preparation (FOP) inhibited arthritic paw edema in rats Twenty-four hours after arthritis induction, we observed a significant increase in the volume of the injected paw in adjuvant-induced arthritis (AIA) control rats, with a progressive increase in edema until day 21
Treatment with 37.5 mg/kg FOP and olive oil (Oo) did not reduce edema in the injected paws or non-injected contralateral paws compared with the AIA group
Summary
Fish oil (FO) is a rich source of n-3 long-chain ( known as omega-3) polyunsaturated fatty acids (PUFAs), especially eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3), and has many health benefits. In adjuvant-induced arthritis (AIA), a plantar injection of Freund’s complete adjuvant (CFA) is an intense and persistent inflammatory stimulus that significantly increases the number of inflammatory cells and the production and release of inflammatory mediators in the affected joint. These events contribute to joint cartilage damage, bone resorption, and other systemic changes in arthritic animals, similar to rheumatoid arthritis in humans (LaBranche et al, 2012). Pharmacological treatment to inhibit the migration and number of leukocytes that are recruited to the joint can reduce local and systemic damage and is an interesting therapeutic intervention
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