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目的:观察沙丁胺醇对正常和IL-13刺激的大鼠支气管平滑肌细胞(rBSMC)胞质Ca2+信号的影响,探讨沙丁胺醇治疗哮喘的作用机制。方法:体外培养大鼠支气管平滑肌细胞,利用共聚焦显微镜测定胞质Ca2+水平,观察沙丁胺醇作用后正常和IL-13刺激后的rBSMC的钙池Ca2+释放和容量性Ca2+内流(CCE)的变化。结果:IL-13 10μg/L处理24 h后,rASMC的Ca2+释放和Ca2+内流均高于正常对照组;10μmol/L沙丁胺醇不影响正常rASMC的Ca2+释放,但是显著抑制CCE;10μmol/L沙丁胺醇对IL-13刺激后的Ca2+释放和CCE的上升均有抑制作用。结论:沙丁胺醇可以抑制Th2细胞因子刺激后的气道平滑肌细胞的容量性Ca2+内流,从而降低胞质Ca2+水平。提示容量性CCE在气道高反应性的发生以及beta 2受体激动剂的治疗效应中具有重要作用。
Objective: To observe the effects of salbutamol on cytoplasmic Ca2 + signal in normal and IL-13-stimulated rat bronchial smooth muscle cells (rBSMCs) and to explore the mechanism of salbutamol treatment of asthma. Methods: The bronchial smooth muscle cells were cultured in vitro. The level of cytoplasmic Ca2 + was measured by confocal microscopy. The changes of Ca2 + release and capacity Ca2 + influx (Ca2 + influx) in normal and IL-13-stimulated rBSMC were observed after salbutamol treatment. Results: Ca2 + release and Ca2 + influx in rASMC were significantly increased after IL-13 treatment at 10μg / L for 24 h. Compared with normal control group, 10μmol / L salbutamol did not affect Ca2 + release in normal rASMC but significantly inhibited CCE and 10μmol / L salbutamol The inhibition of IL-13-induced Ca2 + release and CCE upregulation. Conclusion: Salbutamol can inhibit the Ca2 + influx in airway smooth muscle cells stimulated by Th2 cytokines, thereby reducing the level of cytoplasmic Ca2 +. It is suggested that volumetric CCE plays an important role in the occurrence of airway hyperresponsiveness and the therapeutic effect of beta 2 agonists.