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目的 :深入研究青藤碱对T淋巴细胞Th1类细胞因子表达的影响。方法 :分离小鼠淋巴结细胞 ,加入不同浓度的青藤碱作用 1小时后 ,加多克隆刺激剂PDB和离子霉素 ,继续培养 4小时后收获细胞 ,进行细胞内细胞因子染色 ,以流式细胞术对T细胞Th1类细胞因子TNF γ、炎症性细胞因子TNF α分子表达情况进行分析 ;同时 ,观察药物对T细胞活化早期标志CD6 9表达的影响 ;结果 :10 0 0 μmol L(32 9 2 4 μg ml)青藤碱能够抑制CD6 9表达 ,2 0 0 μmol L青藤碱对CD6 9表达无影响 ;2 0 0、10 0 0、2 0 0 0 μmol L青藤碱能够剂量依赖性地显著降低T细胞内细胞因子TNF γ、TNF α分子表达。 结论 :抑制T细胞活化异常可能是青藤碱治疗类风湿关节炎免疫药理机制之一 ,此抑制效应可能主要不是通过影响PKC而是与影响钙离子依赖的T细胞活化信号传导途径相关。
Objective: To study the effect of sinomenine on the expression of Th1 cytokines in T lymphocytes. METHODS: Mouse lymph node cells were isolated and added with different concentrations of sinomenine for 1 hour. Polyclonal stimulants PDB and ionomycin were added. Cells were further cultured for 4 hours, and cells were intracellularly stained for flow cytometry. The expression of Th1 cytokines TNF γ and TNF α molecules in T cells was analyzed. At the same time, the effects of drugs on CD6 9 expression in early stage of T cell activation were observed. The result was: 100 μmol L (32 9 2 4 μg ml) Sinomenine inhibited the expression of CD69, and 200 μmol L sinomenine had no effect on the expression of CD69; 200, 100, and 200 μmol L Sinomenine could dose-dependently Significantly reduce the expression of cytokines TNF γ and TNF α in T cells. Conclusion : Inhibition of abnormal activation of T cells may be one of the immunopharmacological mechanisms of sinomenine in the treatment of rheumatoid arthritis. This inhibitory effect may not be related to the effect of PKC, but rather to the T cell activation signal transduction pathway that affects calcium ion dependence.