雷公藤抑制致敏小鼠T细胞IL-5mRNA的表达及核因子NFAT活性  

Inhibition of IL-5 mRNA expression and NFAT activity in T lymphocytes in sensitized mice by triptolide

作　　者：程晓明[1] 王长征[1] 钱桂生[1] 

机构地区：[1]第三军医大学新桥医院呼吸疾病研究所,重庆400037

出　　处：《中华微生物学和免疫学杂志》2001年第5期516-519,共4页Chinese Journal of Microbiology and Immunology

基　　金：国家自然科学基金资助项目 ( 39870 946)

摘　　要：目的　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。方法　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NFAT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　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淋巴细胞体外经刀豆蛋白A(ConA)刺激后 ,NFAT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 ,NFAT的DNA结合活性显著减弱。结论　TP抑制IL 5基因转录的分子机制可能与其抑制NFAT的DNA结合活性有关。Objective To explore the effects and mechanisms of triptolide on the expression of IL 5 mRNA in T lymphocytes in sensitized mice. Methods The peritoneal injection and inhalation of ovalbumin (OVA) were used to make sensitized BALB/c mouse model. 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 of NFAT in CD4 +T lymphocytes was assayed by electrophoretic mobility shift assay (EMSA). Results IL 5 mRNA were more intensely expressed on T lymphocytes in sensitized mice than that in the controls ( P <0.01), and were significantly reduced by treatment with triptolide or dexamethasone ( P <0.01). After stimulation by ConA, DNA binding of NFAT in CD4 + T lymphocytes of sensitized mice was more than that in the controls. Change of DNA binding was shown in a time dependent manner. Triptolide and dexamethasone could inhibit the DNA binding of NFAT. Conclusion Suppressed genetic transcription of IL 5 by triptolide or dexamethasone may be explained by the inhibition of NFAT with some unknown mechanisms.

关 键 词：哮喘 雷公藤内酯醇 白细胞介素5 T淋巴细胞 转录因子 

分 类 号：R392.3[医药卫生—免疫学]