Osteoarthritis (OA) is characterized by degradation of matrix and destruction of articular cartilage. Articular chondrocytes are solely responsible for the production and maintenance of the extracellular matrix. Therefore, chondrocyte disruption is implicated in cartilage degeneration. Numerous studies have shown that antioxidant treatments are promising therapeutics in cases of OA. This study was designedto examine whether vitamin E protects rat articular chondrocytes against increased inflammatory markers and oxidative stress and prevents cartilage destruction in mono-iodoacetateinduced osteoarthritis rat model. Data showed that osteoarthritis group showed a significant increase in inflammatory markers, Tumor Necrosis Factor-α (TNF-α) (38±1 ng/mL), Interlukin-6 (IL-6) (253±15 ng/mL) and oxidative stress marker, Super Oxide Dismutase (SOD) (14±1 ng/mL) compared to control (18±1 ng/mL), (121+/-23 ng/mL) and (8±1 ng/mL) respectively. Opposite trend was found when animals were treated with vitamin E where TNF-α (27±2 ng/mL) and SOD (10±1 ng/mL) declined significantly. Electro-microscopic examination documented the above results and showed improvement of knee joint after administration of vitamin E. This study supported the notion that OA is a multi factorial complication, caused by inflammation and increased oxidative stress. Administration of vitamin E decreased the markers of inflammation and oxidative stress as well asimproved ultra-structure of the knee jointin acute OA animal model. However, further work id needed to validate reliability in human patients suffering from osteoarthritis.
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