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目的探讨G蛋白在组胺H3 受体信号转导机制中的作用。方法以高表达组胺H3 受体的垂体细胞瘤AtT 20作为观察系统 ,用放免分析法测定给予H3 受体激动剂后各时间点细胞上清液中ACTH分泌量的变化 ,并观察药物对细胞增殖的影响。结果组胺H3 受体激动剂R (α) MeHA(10 -7mol/L)作用8h ,能明显促进ACTH的释放 ,H1、H2受体激动剂无此作用 ,R (α) MeHA引起ACTH分泌的效应能被H3 受体特异性拮抗剂thioperamide所拮抗 ,而H1 受体和H2 受体拮抗剂均不影响R (α) MeHA的效应。用G蛋白失活剂NEM预处理细胞后 ,取消了R α MeHA增强AtT 20细胞分泌ACTH的效应。结论特异性激动组胺H3 受体后能引起兴奋 分泌偶联过程 ,其信号转导过程中有G蛋白的参与。
Objective To investigate the role of G protein in histamine H3 receptor signal transduction mechanism. METHODS: Pituitary cell tumor AtT 20 with high expression of histamine H3 receptor was used as an observation system. Changes in ACTH secretion in cell supernatants at various time points after H3 receptor agonist administration were determined by radioimmunoassay, and drug-paired cells were observed. The effect of proliferation. Results The action of histamine H3 receptor agonist R (α) MeHA (10 -7 mol/L) for 8 h significantly promoted the release of ACTH. H1 and H2 receptor agonists did not, and R (α) MeHA caused ACTH secretion. The effect can be antagonized by H3 receptor-specific antagonist thioperamide, and neither H1 receptor nor H2 receptor antagonist affects the effect of R(α)MeHA. Pretreatment of cells with the G protein inactivator NEM eliminated the effect of R α MeHA on the secretion of ACTH from AtT 20 cells. Conclusion The specific activation of histamine H3 receptor can induce the excitatory secretion coupling process, and G protein is involved in the signal transduction process.