Department of Pathology, University of Adelaide, 5005, Adelaide, SA.
Inflammopharmacology. 1998;6(3):193-202. doi: 10.1007/s10787-998-0019-z.
This 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-gamma 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.
本研究比较了替尼达普、吡罗昔康和环孢素 A（CsA）在大鼠佐剂性关节炎模型中的抗关节炎活性。本研究的目的是将替尼达普的任何疾病改善作用与其体内对细胞因子的调节作用相关联。替尼达普和吡罗昔康均在关节炎表现出最初迹象时开始口服给药，可减轻关节炎疾病。疾病抑制与白细胞介素-6 产生的显著减少以及白细胞介素-1 和肿瘤坏死因子产生的轻微减少相关。当与佐剂共同给药时，替尼达普和 CsA 分别预防了 50%和 100%的动物发生疾病，而吡罗昔康则没有效果。替尼达普和 CsA 诱导的这种疾病预防与佐剂性疾病开始后一天淋巴结细胞中干扰素-γ和白细胞介素-2 产生的减少相一致。这种 T 细胞细胞因子的抑制作用可能与替尼达普作为一种疾病改善药物有关。
