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目的:观察BRS-3激活对人支气管上皮细胞凋亡的影响,以探讨BRS-3在气道功能稳态中的生物学作用,进一步拓展对神经源性气道高反应性机制的认识。方法:人支气管上皮细胞常规培养,流式细胞仪检测细胞凋亡。结果:臭氧应激促进支气管上皮细胞凋亡,BRS-3激活可抑制臭氧应激诱导的细胞凋亡。结论:BRS-3激活抑制细胞凋亡,提示BRS-3激活维持应激状态下支气管上皮细胞功能稳态,可能在哮喘等气道高反应性疾病中起保护作用。
OBJECTIVE: To observe the effect of BRS-3 activation on the apoptosis of human bronchial epithelial cells in order to explore the biological role of BRS-3 in airway homeostasis and to further understand the mechanism of neurogenic airway hyperresponsiveness. Methods: Human bronchial epithelial cells were cultured routinely, and apoptosis was detected by flow cytometry. Results: Ozone stress promoted bronchial epithelial cell apoptosis. BRS-3 activation inhibited apoptosis induced by ozone stress. CONCLUSIONS: BRS-3 activation inhibits apoptosis, suggesting that BRS-3 activation maintains the homeostasis of bronchial epithelial cells under stress and may play a protective role in airway hyperresponsiveness diseases such as asthma.