N-Dimethyl chalcone facilitated augmentation of IL-10 and diminution of TNF-α, IL-1β, IL-6, NFκB, and COX-2 in FCA-induced arthritic rat model.

Abstract

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent inflammation and chronic pain due to the degradation of subchondral bone and the loss of cartilage function. The present study was designed to evaluate the activity of 1N,N-dimethyl chalcone (DGCHAL) against RA. A primary 28-day investigation was conducted on adjuvant-induced arthritic rats with DGCHAL (10 mg/kg, 20 mg/kg, and 30 mg/kg) and methotrexate (STDMTX). The therapeutic effect was estimated on the basis of measurements of paw diameter, fluctuations in body weight, oxidative stress biomarkers, and hematological parameters. In addition, the study sought to quantify the expression of key cytokines, including TNFα, IL-6, IL-10, IL-1β, and NFκβ, using qRT-PCR and ELISA techniques. Treatment with DGCHAL significantly restored the paw volume, body weight, arthritis-induced anemia, and leukocyte count. The tested compound remarkably downregulated the expression of COX-2, TNFα, IL-6, IL-1β, and NFκB and upregulated the expression of IL-10. The treatment groups increased the activities of SOD, CAT, and GSH, whereas they reduced the formation of MDA and NO as compared to the arthritic group. These findings provide an evident basis for the anti-arthritic potential of DGCHAL in a chronic arthritis rat model and should be further studied for dosage form design.