胶原性关节炎大鼠血清中TNF-α，IL-17及IL-10水平分析

Analysis of TNF-α, IL-17 and IL-10 levels in the serum of rats with collagen-induced arthritis

关键词:  胶原性关节炎  TNF-α  IL-17  IL-10  关节炎症指数

Key words:  collagen-induced arthritis  TNF-α  IL-17  IL-10  arthritis index

摘要:

[目的] 检测血清TNF-α，IL-17及IL-10在Ⅱ型胶原诱导性关节炎（CIA）大鼠血清中的表达。[方法]建立CIA动物模型，用酶联免疫吸附实验(ELISA)法检测大鼠模型血清中炎性细胞因子TNF-α、IL-10 及IL-17的水平，同时观察大鼠炎症指数。[结果]60只大鼠随机被分为造模组(40只)和对照组(20只)，免疫4周后，造模组40只大鼠有32只发病。造模成功组大鼠血清中TNF-α、IL-17水平分别为(39.65±11.23)pg/mL和(46.1±10.9)pg/mL，明显高于造模失败组和正常对照组(P 均<0.05)，而IL-10水平(29.11±27.59)pg/mL明显低于造模失败组和正常对照组(P<0.05)。另外，造模组大鼠血清TNF-α和IL- 17水平与CIA大鼠炎症指数呈正相关关系(r=0.573, r=0.492, P<0.05)，与之相反，CIA大鼠血清IL-10水平与炎症指数呈负相关关系(r=-0.481, P<0.05)。[结论]致炎因子(TNF-α, IL-17)和抑炎因子(IL-10)表达失衡可能在CIA发病中具有重要作用。

Abstract:

[Objective] To investigate the serum levels of TNF-α, IL-17 and IL-10 in rats with type II collagen-induced arthritis(CIA). [Methods] The rat model was established using type II collagen and the serum levels of TNF-α, IL-17 and IL-10 were determined by enzyme-linked immunosorbent assay(ELISA)．The arthritis index in CIA rats were observed. [Results] Sixty rats were randomized into two groups：modeling group (40 rats) and normal control (20 rats). After 4 weeks, the models of CIA were established in 32 rats. The serum levels of TNF-α and IL-17 in the successful modeling group were (39.65±11.23)pg/mL and (46.1±10.9)pg/mL, respectively, significantly higher than that in the abortive modeling group and normal control. While serum concentration of IL-10(29.11±27.59)pg/mL in the successful modeling group was remarkably lower than that in the abortive modeling group and normal control (P<0.05). In addition, There were positive correlations between TNF-α, IL-17 and arthritis index (r=0.573, r=0.492, P<0.05), negative correlations between IL-10 and arthritis index in CIA rats (r=-0.481, P<0.05). [Conclusion] The imbalance of pro- inflammatory cytokine (TNF-α, IL-17) and anti-inflammatory cytokine (IL-10) network may be playing an important role in the pathogenesis of CIA．