雷公藤对致敏小鼠T细胞IL-5 mRNA表达及转录因子GATA-3活性的抑制作用

探讨雷公藤内酯醇 (TP )对致敏小鼠T淋巴细胞IL 5mRNA表达的影响及其机制。采用卵蛋白 (OVA )致敏的方法建立模型 ;运用原位杂交染色法 (ISH )观察TP对T淋巴细胞IL 5mRNA表达的影响 ;通过凝胶电泳迁移率实验 (EMSA )对CD4+T淋巴细胞核转录因子GATA 3的DNA结合活性进行检测 ,同时就TP的作用与地塞米松 (DM )相比较。结果表明致敏小鼠T淋巴细胞IL 5mRNA表达显著高于正常对照组 (P <0 0 1) ,经TP、DM处理后 ,其IL 5mRNA表达显著低于致敏组(P <0 0 1)。致敏小鼠CD4+ T淋巴细胞体外经伴刀豆蛋白A (ConA )刺激后 ,GATA 3的DNA结合活性与正常对照组比较显著增强 ,并呈时间依赖关系 ,经TP、DM处理后 ,GATA 3的DNA结合活性显著减弱。TP抑制IL 5基因转录的分子机制可能与其抑制GATA 3的DNA结合活性有关。

Inhibitory Effect of Triptolide on the Expression of IL-5 mRNA and the Activities of Transcription Factor GATA-3 in T Lymphocytes of Sensitized Mice

To explore the effects and mechanisms of triptolide on the expression of IL-5 mRNA in T lymphocytes in sensitized mice,the peritoneal injection and inhalation of ovalbumin(OVA) were used to produce the sensitized Balb/c mouse model,and in situ hybridization (ISH) was adapted to explore the expression of IL-5 mRNA and the effects of triptolide and dexamethasone in T lymphocytes. The DNA-binding activity of GATA-3 in CD4 T lymphocytes was assayed by using electrophoretic mobility shift assay (EMSA). It was found IL-5 mRNA were expressed more intensely in T lymphocytes in sensitized mice than that in the normal controls (P<0.01),and were significantly reduced by treatment with triptolide or dexamethasone (P<0.01). After stimulated with ConA,DNA-binding activities of GATA-3 in CD4 T lymphocytes of sensitized mice were higher than that in the normal controls. Changes of DNA-binding activities were ina time-dependent manner. Triptolide and dexamethasone could inhibit the DNA-binding activities of GATA-3. Molecular mechanisms for the suppressed genetic transcription of IL-5 by triptolide or dexamethasone may be involved in the inhibition of GATA-3.