Haynes, D.Hutchens, M.Whitehouse, M.Vernon-Roberts, B.2006-06-232006-06-231998Inflammopharmacology: experimental and clinical studies, 1998; 6(3):193-2020925-46921568-5608http://hdl.handle.net/2440/5644This study compared the antiarthritic activity of tenidap, piroxicam and cyclosporin-A (CsA) using the model of adjuvant-induced arthritis in rats. The aim of the study was to correlate any disease-modifying effects of tenidap with its in-vivo regulation of cytokines. Both tenidap and piroxicam reduced arthritic disease when administered orally from the time the first signs of arthritis are expressed. Disease suppression correlated with a significant reduction in interleukin-6 production and a slight reduction in interleukin-1 and tumour necrosis factor production. When coadministered with the adjuvant, tenidap and CsA prevented disease in 50% and 100% of animals, respectively, whereas piroxicam had no effect. This disease prevention induced by tenidap and CsA coincided with reduced interferon-γ and interleukin-2 production by lymph node cells one day following initiation of adjuvant disease. This inhibition of T-cell cytokines might be consistent with tenidap acting as a disease-modifying drug.en© Springer, Part of Springer Science+Business MediaJournal article0030006181001998101210.1007/s10787-998-0019-z2-s2.0-003175560570187