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目的:初步探讨神经肽P物质刺激肥大细胞脱颗粒的神经调控机制。方法:分A、B两组进行体外诱导小鼠骨髓肥大细胞。A组培养液中加入SCF、IL-3和IL-4,B组培养液中加入SCF、IL-3诱导分化,培养4周后收集细胞备用。Western Blot分析各组骨髓肥大细胞FcεRⅠα和NK-1R表达情况。两组分别加入不同浓度神经肽P物质孵育30min,检测上清液和细胞内组胺含量,计算组胺释放率。结果:A组FcεRⅠα和NK-1R的表达均较B组高(P<0.05);P物质可促发A、B两组肥大细胞脱颗粒,且同一浓度P物质刺激时,A组肥大细胞脱颗粒程度高于B组(P<0.05)。结论:P物质介导的肥大细胞脱颗粒的神经调控机制可能存在由其特异受体NK-1R介导的非免疫性及FcεRⅠα介导的免疫性双途径,为深入研究鼻黏膜高反应性鼻病的发病机制以及临床治疗策略提供了新思路。
Objective: To investigate the neuromodulatory mechanism of neuropeptide P-stimulated mast cell degranulation. Methods: A and B groups were divided into two groups to induce mouse bone marrow mast cells in vitro. SCF, IL-3 and IL-4 were added to group A, SCF was added into group B, IL-3 was induced to differentiate, and cells were collected after 4 weeks. Western Blot analysis of each group of bone marrow mast cells FcεR Ⅰ α and NK-1R expression. Two groups were added different concentrations of neuropeptide substance P incubated 30min, the supernatant and intracellular histamine content was measured to calculate histamine release rate. Results: The expression of FcεRⅠα and NK-1R in group A was higher than that in group B (P <0.05). Substances of substance A and B could induce the degranulation of mast cells in group A and B, and when the same concentration of substance P was stimulated, The degree of granules was higher than that of group B (P <0.05). CONCLUSIONS: The substance-mediated mast cell degranulation may have dual pathways of NK-1R-mediated non-immunity and FcεRI-mediated immunity. It is necessary to further study the nasal mucosa highly reactive nasal Disease pathogenesis and clinical treatment strategies provide a new idea.