Abstract
Tocotrienols exhibit a significant anti-inflammatory and antioxidant effect in numerous human diseases. However, the anti-inflammatory and antioxidant effects of tocotrienols in arthritic conditions are not well documented. Therefore, the effect of γ-tocotrienol supplementation against oxidative stress and joint pathology in collagen-induced arthritis in rats was investigated in the present study. Adult female Dark Agouti rats were randomly divided into groups: Control, γ-tocotrienol alone, arthritis alone and arthritis with γ-tocotrienol. Arthritis was induced using 4 mg/kg body weight collagen in complete Freund’s adjuvant. The rats were treated orally with 5 mg/kg body weight of γ-tocotrienol between day 21 and day 45. After 45 days, serum C-reactive protein (CRP), tumor necrosis factor (TNF)-α, superoxide dismutase (SOD) and total glutathione (GSH) assays were conducted. γ-tocotrienol significantly reduced the arthritis-induced changes in body weight, CRP, TNF-α, SOD and the total GSH levels. There was a significant reduction in the arthritis-induced histopathological changes in the γ-tocotrienol treatment group. The data indicated that administration of γ-tocotrienol resulted in a significant antioxidant and anti-inflammatory effect on collagen-induced arthritis; therefore, γ-tocotrienol may have therapeutic potential as a long-term anti-arthritic agent in rheumatoid arthritis therapy.
Highlights
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease that is associated with progressive disability and systemic complications [1,2]
The present study demonstrated that γ‐tocotrienols are an effective inhibitor of arthritis‐induced oxidative stress and tumor necrosis factor (TNF)‐α secretion
Female Dark Agouti rats, aged 6‐10 weeks, were injected with type II collagen emulsified with Complete Freund's adjuvant (CFA), which induced an immunological hypersensitivity reaction to the collagen within the rats, leading to the development of chronic inflammatory arthritis
Summary
Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease that is associated with progressive disability and systemic complications [1,2]. Other joints that are commonly affected include the hips, knees, ankles, feet, neck, shoulders and elbows. In addition to joint pain and inflammation, individuals suffering from RA may experience fatigue, occasional fevers and a general sense of ill health [2,3,4]. The cellular and molecular pathology of RA involves chronic inflammation of the synovium as well as synovial proliferation and infiltration by macrophages, memory T cells and plasma cells. Regardless of recent improvements in the treatment options for RA, the pathology underlying inflammatory arthritis and its causative factors have not been well described
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