中文摘要：

目的 探讨羧胺三唑对TNF-α诱导的佐剂性关节炎大鼠成纤维样滑膜细胞分泌促炎细胞因子的影响及部分机制.方法 用弗氏完全佐剂诱导大鼠佐剂性关节炎模型,分离培养的佐剂性关节炎成纤维样滑膜细胞用20 ng/ml TNF-α刺激并用不同浓度羧胺三唑（10、20、40 μmol/L）处理.ELISA法检测成纤维样滑膜细胞上清中IL-1β和IL-6含量,Western blot法检测NF-KB p65的蛋白表达.结果 经20 ng/mlTNF-α刺激后,成纤维样滑膜细胞分泌IL-1β和IL-6水平,以及细胞核中NF-KB p65的表达显著增加（P＜0.01）.羧胺三唑（20、40 μmol/L）能够显著抑制TNF-α诱导的IL-1β[（417.39 ＋29.80） pg/mlvs.（264.63±9.35） pg/ml,（186.13±25.71）pg/ml,P ＜0.01]和IL-6[（383.45±32.13） pg/ml vs.（248.39±30.51） pg/ml,（189.64±27.86） pg/ml,P＜0.01]分泌,且明显减少细胞核中NF-κB p65的表达（P＜0.01）.结论 羧胺三唑可能通过抑制NF-KB活化来减少TNF-α诱导的佐剂性关节炎成纤维样滑膜细胞中促炎细胞因子IL-1β、IL-6的产生.

英文摘要：

Objective To investigate the effects of carboxyamidotriazole （CAI） on TNF-α-induced cytokines secretion in fibroblast-like synoviocytes （FLS） from adjuvant arthritis （AA） rats and its mechanisms.Methods Freund＇s completed adjuvant was used to induce AA in rats.FLS from AA rats were stimulated with 20 ng/ml TNF-α and incubated with CAI at the concentrations of 10,20,40 μmol/L.The contents of IL-1β and IL-6 in the culture supernatant were determined by ELISA method,and the expression of NF-κB p65 in the cell nucleus was measured by Western blot.Results TNF-α significantly increased the secretion of IL-1β and IL-6,and the nuclear expression of NF-κB p65 in the FLS （P ＜ 0.01）.CAI （20,40 μmol/L） inhibited the productions of IL-1β [（417.39 ± 29.80） pg/ml vs.（264.63 ± 9.35） pg/ml,（186.13 ± 25.71） pg/ml,P ＜ 0.01] and IL-6 [（383.45 ±32.13） pg/ml vs.（248.39 ± 30.51） pg/ml,（189.64 ± 27.86） pg/ml,P ＜ 0.01] in TNF-α-induced FLS,and CAI （20,40 μmol/L）also inhibited NF-κB p65 expression in the nucleus of TNF-ot-induced FLS （P ＜ 0.01）.Conclusion CAI attenuate the secretion of pro-inflammatory cytokines such as IL-1β and IL-6 through inhibiting the activation of NF-kB.