Methionine attenuates the intensity of rheumatoid arthritis by downregulating NF-κB and iNOS expression in neonatal rats.

Abstract

The present study investigated the anti-arthritic effects of methionine in neonatal rats. Rats were divided into four groups, with six rats in each group. The rats were administered methionine (150- or 300-mg/kg body weight) orally for 45 consecutive days. The expression levels of catalase, superoxide dismutase (SOD), reduced glutathione (GSH), lipid peroxidation, glutathione peroxidase (Gpx), prostaglandin E2 (PGE2), matrix metalloproteinase-3, uric acid, nitric oxide (NO), ceruloplasmin, inducible nitric oxide synthase (iNOS), and nuclear factor (NF)-κB were determined in rheumatoid arthritis-induced neonatal rats. The levels of SOD, catalase, Gpx, and GSH were substantially reduced in control rats, while the levels of other parameters were increased in control neonatal rats. However, methionine supplementation significantly increased (more than 40%) the levels of SOD, catalase, Gpx, and GSH in neonatal rats. The levels of lipid peroxidation, uric acid, ceruloplasmin, NO, and PGE2 were significantly reduced following methionine supplementation. Furthermore, NF-κB mRNA expression was substantially reduced up to 51.7% in the 300-mg/kg methionine group, whereas the mRNA expression of iNOS was reduced up to 43.5% in the 300-mg/kg methionine group. NF-κB protein expression was substantially reduced up to 45.8% in the 300-mg/kg methionine group, whereas the protein expression of iNOS was reduced up to 45.4% in the 300-mg/kg methionine group. Taken together, these data suggest that methionine supplementation was effective against rheumatoid arthritis.