Effect of allopurinol and vitamin e on rat model of rheumatoid arthritis

Rat collagen II-induced arthritis is a model of chronic inflammation induced by mycobacterium butyricum and collagen II. It is characterized by similar pathophysiological and pathobiochemical changes as rheumatoid arthritis (RA) in humans. In the present study, the biochemical effects of vitamin E and allopurinol (Allo) on RA of rats were investigated.

Forty male rats were divided into four groups (10 rats each): control group, collagen II-induced RA group (CII group), CII group treated with allopurinol (CII+ Allo), and CII group treated with vitamin E (CII + Vit E). After 6 weeks of treatment, the plasma levels of lipid peroxides (LPO), nitric oxide (NO), ceruloplasmin (CP), superoxide dismutase (SOD), uric acid (UA) and glutathione (GSH) were detected using colorimetric methods. The plasma levels of PGE2 were measured using ELISA assay. The plasma levels of copper (Cu) and zinc (Zn) were determined using atomic absorption spectrometer.

In CII treated group, the levels of LPO, NO, PGE2, UA, CP and Cu were significantly higher, but the levels of SOD, GSH and Zn were significantly lower than controls. In CII + Allo treated group, the levels of SOD and GSH were significantly increased, but the levels of PGE2, LPO, NO, UA, Cu and CP were significantly decreased in comparison with CII-treated group. The levels of SOD, GSH and Zn were significantly increased, but the levels of PGE2, NO and CP were significantly decreased in the vitamin E treated group in comparison with CII-treated group. The levels of PGE2, LPO, Cu and Zn were significantly lower in vitamin E treated group than Allo-treated group. In conclusion, the study suggests that proper antioxidant intake management may reduce free radical generation and improve antioxidant status in RA. Allopurinol and vitamins E may effectively normalize in different degrees the impaired the oxidant/antioxidant system and may be useful in delaying the complication of RA. Moreover, they display anti-inflammatory action by decreasing PGE2 level in RA.