15d-PGJ2 ameliorates the inflammatory process on rheumatoid arthritis-induced into rats’ temporomandibular joint (CAM5P.240)

Abstract

Abstract The aim of this study was to evaluate the peripheral effect of 15d-PGJ2 in Rheumatoid Arthritis-induced inflammation in the temporomandibular joint (TMJ) of rats. Antigen-induced arthritis (AIA) was generated in rats with methylated bovine serum albumin (mBSA) diluted in complete Freund's adjuvant. Pretreatment with an intra-articular injection of 15d-PGJ2 (100 ng/TMJ) before mBSA intra-articular injection (10 µg/TMJ) (challenge) in immunized rats significantly reduced the RA-induced hypernociception (p<0.05; ANOVA, Tukey test). Corroborating these results, 15d-PGJ2 was able to inhibit plasma extravasation, leukocyte migration and the release of inflammatory cytokines TNF-α, IL-1β, IL-6, IL-12, IL-18 and the chemokine KC and CINC-1 (p<0,05: ANOVA, Tukey Test). Moreover, the effect of 15d-PGJ2 to increase the decay accelerating factor (CD55) expression associated to decrease pro-inflammatory cytokines release may explain the inhibition of leukocyte infiltration, through a shift in the balance of the pro- and anti-adhesive properties. To confirm these results histopathological analysis showed that 15d-PGJ2 reduced the inflammatory parameters induced by RA. Thus, 15d-PGJ2 might be used as a potential anti-inflammatory drug to treat RA inflammation of the temporomandibular joint.