Objective To analyze the interaction and possible signal transduction pathways of tumor necrosis factor-α (TNF-α) and osteopontin ( OPN) in expression of synovial fibroblasts of rheumatoid arthritis. Methods Collagen-induced arthritis (CIA) model was induced by bovine II collagen and incomplete Freund's adjuvant. The synovial membrane of the normal control group and model group were taken to culture synovial fibroblasts cells (SFs) by collagenase digestion. The SFs were divided into control group, model group, model group + lipopolysaccharide ( LPS) , model group + LPS + p38 channel inhibitor (SB203580). The levels of OPN mRNA were evaluated, and the interaction and possible signal transduction pathways between TNF-a and OPN were analyzed. Results LPS significantly increased the expression of OPN mRNA in model group cells (P <0. 01 ) , the addition of SB203580 significantly reduced the expression of OPN mRNA. There were significant differences among the 4 groups (P <0.01). Conclusion TNF-a can induce the expression of OPN, and this process are able to realize through p38 mitogen activated protein kinase (p38MAPK) signal transduction pathway.%目的 分析肿瘤坏死因子-α(TNF-α)和骨桥蛋白(OPN)在类风湿关节炎滑膜成纤维细胞中表达的相互影响及可能的信号转导途径.方法 采用牛源性Ⅱ型胶原配合不完全弗氏佐剂制造胶原诱导性关节炎(CIA)模型,取正常对照组和模型组膝关节滑膜,胶原酶消化法分别培养滑膜成纤维细胞(SFs),分成正常对照组、模型组、模型组+脂多糖(LPS)、模型组+LPS+ p38途径抑制剂(SB203580),观察SFs中OPN mRNA的变化,分析TNF-α与OPN表达的相互影响及可能的信号转导途径.结果 模型组细胞加入LPS刺激后OPN mRNA表达较模型组明显增多(P＜0.01),予SB203580后,OPNmRNA的表达显著减少,4组间比较差异显著(P＜0.01).结论 TNF-α可诱导OPN的表达,这一过程可能是通过p38丝裂原活化蛋白激酶(p38 MAPK)信号转导途径而实现的.
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