雷公藤甲素对CIA大鼠γδT细胞胞内细胞因子表达的影响

Effects of Triptolide on the Expressions of Intracellular Cytokines of the γδT Lymphocyte in the Rat with Collagen-Induced Arthritis

目的 观察雷公藤甲素对II型胶原诱导的关节炎 (CIA)大鼠外周血γδT细胞表达细胞因子TNF α和IL 10的影响 ,探讨γδT细胞在CIA中的作用机制和雷公藤甲素对γδT细胞的免疫调节作用。方法 Wistar大鼠背部及尾根部多点皮内注射牛Ⅱ型胶原诱导CIA动物模型 ,大鼠经雷公藤甲素治疗后 ,取外周血分离淋巴细胞 ,用流式细胞仪 ,通过直接荧光标记的抗TNF α和抗IL 10抗体来检测单个细胞水平γδT细胞胞内细胞因子的表达。结果 CIA模型大鼠外周血中γδT细胞与正常大鼠相比较 ,所占淋巴细胞的百分比显著下降 (6 96± 0 74 ) % ,γδT细胞胞内TNF α(2 2 2±0 36 ) %和IL 10 (1 0 0± 0 2 0 ) %的表达均明显降低 (P <0 0 1)。通过雷公藤甲素治疗后 ,γδT细胞的数量和TNF α与IL 10的表达均恢复至正常水平。结论 雷公藤甲素可调节CIA大鼠外周血γδT细胞的数量和TNF α及IL 10表达水平 。

Objective To observe the effects of triptolide on the expressions of TNF-α and IL-10, the two cytokines of γδT lymphocytes in the peripheral blood of the rat with collagen-induced arthritis (CIA) in order to investigate the behavior of the γδT lymphocytes in CIA and the immunoregulation of triptolide over the γδT lymphocytes.Methods Wistar rats were used to induce the animal model of CIA by intradermally injecting bovine type II collagen at the back and the root of the tail. After being treated with triptolide, the peripheral blood was taken from the model rat for separating γδT lymphocytes. The flow cytometer and the TNF-α and IL-10 antibodies directly labeled with fluorescence were used to detect the expression of the intracellular cytokines of the γδT lymphocytes at the single-cell level. Results The percentage of γδT lymphocytes, (6.96±0.74)%, in the total lymphocytes; the percentage of the expression of intracellular TNF-α of γδT lymphocytes; (2.22±0.36)%; and the percentage of the expression of intracellular of IL-10, (1.00±0.20)%; were markedly decreased in the peripheral blood of the model rats, as compared with those in the normal control rats (P<0.01). After the treatment with triptolide, all the three above-mentioned criteria were restored to their normal level. Conclusion Triptolide can exert an effect for treating rheumatoid arthritis, of which the mechanism may be its regulating the amount of γδT lymphocytes and the expressions of TNF-α and IL-10.