摘要
目的 探讨雷公藤对哮喘豚鼠模型IL 5、GM CSF表达的影响及其机制。方法 采用卵蛋白 (OA)致敏复制哮喘豚鼠模型 ,用原位杂交 (ISH)就雷公藤甲素 (TP)对其肺组织和外周血单个核细胞 (PBMC)IL 5、GM CSFmRNA表达的影响进行检测。并通过凝胶电泳迁移试验 (EMSA)检测TP对伴刀豆蛋白 (ConA)或佛波脂 (PMA)刺激的人T细胞核因子 κB(NF κB)的DNA结合活性的影响。结果 哮喘豚鼠肺组织和PBMCIL 5、GM CSFmRNA表达显著高于正常组 (P <0 0 1)和TP处理组 (P <0 0 5或 0 0 1)。ConA或PMA刺激可使T细胞NF κB的DNA结合活性增强 ,活性增强的NF κB为多克隆抗体P6 5和P5 0的异源二聚体 ,TP可以降低该NF κB的DNA结合活性。结论 雷公藤通过抑制NF κB的DNA结合活性 ,进而抑制IL 5、GM CSFmRNA的转录 ,可能是其治疗哮喘的机制之一。
Objective To investigate the effects of triptolide on the expressions of IL 5, GM CSF of asthma. Methods The allergic guinea pigs were induced by ovalbumin. IL 5 and GM CSF mRNA expressions in lung tissue and peripheral blood mononuclear cells (PBMC) of allergic guinea pigs were detected by in situ hybridization. At the same time, the effects of triptolide on DNA binding activities of nuclear factor kappa B (NF κB) of human T cells stimulated by concanavalin A (Con A) or phorbol myristate acetate (PMA) were detected by electrophoretic mobility shift assay (EMSA). Results 1. By comparing with the normal controls, the expressions of IL 5, GM CSF mRNA in lung tissue and PBMC of allergic guinea pigs were significantly higher. Treatment with triptolide could markedly inhibit IL 5, GM CSF mRNA expressions ( P <0.05 or P <0.01). 2. Triptolide could inhibit NF κB DNA binding activities of T cells stimulated with ConA or PMA. Conclusion One mechanism of T. Wilfordii Hook.f. for asthma therapy is its inhibition on transcription of IL 5 and GM CSF genes by inhibition on activities of NF κB.
出处
《中华微生物学和免疫学杂志》
CAS
CSCD
北大核心
2001年第1期66-69,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 )
