IL-17、IL-23、IL-6、TGF-β1和Foxp3在实验性结肠炎中的表达

Expressions of IL-17,IL-23,IL-6,TGF-β1 and Foxp3 on TNBS-induced experimental colitis in rats

目的观察2、4、6-三硝基苯磺酸(TNBS)诱导的大鼠结肠炎模型中结肠Foxp3、TGF-β1的表达及外周血清IL-17、IL-23和IL-6的表达,以探讨Th17细胞在IBD的作用。方法10只SD大鼠以三硝基苯磺酸(TNBS)/乙醇溶液灌肠诱导结肠炎模型。另取10只大鼠作为正常对照组(0.9%NaCl溶液灌肠)。干预2周后行结肠大体损伤指数(CMDI)和组织学损伤指数(TDI)评分,以酶联免疫吸附测定(ELISA)检测血清白介素-6(Interleukin6,IL-6)、IL-17和IL-23水平,以免疫组化方法(SP法)检测结肠组织转化生长因子-β1(TGF-β1)和叉头样转录因子-3(Foxp3)表达。结果与正常组相比,结肠炎模型组CMDI和TDI显著升高(P<0.01),血清IL-6、IL-17和IL-23水平明显升高(P<0.05),结肠组织TGF-β1和Foxp3明显降低(P<0.05)。结论在TNBS诱导的大鼠实验性结肠炎中,IL-6可能通过介导T细胞向Th17或Treg细胞的分化,促进或抑制肠道炎症。

Objective To study the expressions of IL-17,IL-23,IL-6,TGF-β1 and Foxp3 on experimental colitis in rats.Methods Colitis models in 10 rats were induced by rectal administration of trinitrobenzene sulfonic acid （TNBS）dissolved in ethanol,served as model control group.Other 10 rats receiving 0.9% NaCl solution served as normal controls.After 2-week,the colonic macroscopic damage index （CMDI） and tissue damage index （TDI） were evaluated,the serum levels of interleukin-6 （IL-6）,IL-17 and IL-23 were determined by enzyme-linked immunosorbent assay （ELISA）,and the colonic expressions of TGF-β1 and Foxp3 were determined by immunehistochemical method.Results Compared with normal control group,CMDI and TDI in model group increased significantly （P〈0.01）;the serum level of IL-6,IL-17 and IL-23 in model group increased significantly,the colonic expressions of TGF-β1 and Foxp3 in model group decreased significantly （P〈0.05）.Conclusion In TNBS-induced experimental colitis rats,IL-6 may play a key role in inducing or inhibiting inflammation through inducing Th17 cells or Treg differentiation.