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目的初步探讨地塞米松对聚肌胞苷酸刺激气道上皮细胞后趋化因子表达的影响及其机制。方法将人气道上皮细胞16hBE给予不同浓度的聚肌胞苷酸(0.001、0.01、0.1、1μg/ml)及地塞米松(0.1、1、10μmol/L)处理,用RT-PCR检测刺激6 h后IL-8、IP-10 mRNA的表达水平,用ELISA法检测刺激24 h后培养上清液中IL-8和IP-10蛋白含量,用免疫组化方法检测细胞NF-κB p65亚单位的表达强度。结果0.001、0.01、0.1μg/ml聚肌胞苷酸处理16hBE细胞后IL-8和IP-10 mRNA表达水平和蛋白分泌量呈浓度依赖性升高,在0.01μg/ml及0.1μg/ml浓度时,与对照组比较差异有统计学意义(P<0.05,P<0.01);但在聚肌胞苷酸浓度为1μg/ml时,IL-8和IP-10 mRNA表达水平和蛋白分泌量都出现了下降。地塞米松(1、10μmol/L)预处理0.5 h明显抑制聚肌胞苷酸诱导的IL-8和IP-10 mRNA表达及蛋白分泌(P<0.05,P<0.01)。1μmol/L地塞米松预处理明显抑制了聚肌胞苷酸诱导的NF-κB p65表达强度(P<0.01)。结论糖皮质激素可抑制聚肌胞苷酸诱导的气道上皮细胞趋化因子的表达,其机制可能与NF-κB的活化有关。
Objective To investigate the effect and mechanism of dexamethasone on the expression of chemokines after poly-cytidine stimulation of airway epithelial cells. Methods Human airway epithelial cells were treated with different concentrations of polymyosine (0.001, 0.01, 0.1 and 1 μg / ml) and dexamethasone (0.1, 1 and 10 μmol / L) for 16 h. The expression of IL-8 and IP-10 mRNA was detected by ELISA. The content of IL-8 and IP-10 in supernatant of culture supernatants were detected by ELISA, and the expression of NF-κB p65 subunit was detected by immunohistochemistry Expressive intensity. Results The expression levels of IL-8 and IP-10 mRNA and the protein secretion increased in a concentration-dependent manner after being treated with 0.001, 0.01 and 0.1 μg / ml poly-cytidylic acid for 16 hBE cells. At concentrations of 0.01 μg / ml and 0.1 μg / ml (P <0.05, P <0.01). However, at the concentration of 1 μg / ml, IL-8 and IP-10 mRNA expression levels and protein secretion were both higher than those in the control group There has been a decline. 0.5 h pretreatment with dexamethasone (1, 10 μmol / L) significantly inhibited polymyxin-induced IL-8 and IP-10 mRNA expression and protein secretion (P <0.05, P <0.01). Pretreatment with 1 μmol / L dexamethasone significantly inhibited poly (myosinic acid) -induced NF-κB p65 expression (P <0.01). Conclusion Glucocorticoid can inhibit polymyxin-induced chemotactic factor expression in airway epithelial cells, which may be related to the activation of NF-κB.