糖皮质激素调节JAK2/STAT5信号抑制小鼠气道重塑平滑肌细胞的增殖作用

Effect of Glucocorticoid Regulating JAK2/STAT5 Signal on Proliferation of Smooth Muscle Cells in Mice with Airway Remodeling

目的观察糖皮质激素(glucocorticoid,GCS)通过调节JAK2/STAT5信号通路,抑制小鼠气道重塑气道平滑肌细胞增殖的作用。方法以卵白蛋白致敏和雾化激发制备慢性小鼠哮喘气道重塑模型,计数支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)中嗜酸性粒细胞(eosinophil,EOS)占白细胞总数的百分比;肺组织切片HE染色观察小鼠气道平滑肌厚度的病理改变;Western Blot检测肺组织中磷酸化p-JAK2和p-STAT5的蛋白表达。结果糖皮质激素能显著降低哮喘模型小鼠BALF中EOS的百分比(P<0.05);糖皮质激素组小鼠气道平滑肌厚度低于模型组(P<0.05);糖皮质激素能显著降低p-JAK2和p-STAT5的蛋白表达(P<0.05)。结论糖皮质激素能通过调节JAK2/STAT5信号通路够有效缓解小鼠气道重塑气道平滑肌细胞增殖的作用,具有一定的气道保护作用。

Objective To observe the effect of glucocorticoid （GCS） on the proliferation of airway smooth muscle cells in mice by regulating JAK2 / STAT5 signaling pathway.Methods The model of airway remodeling in chronic mice was established by ovalbumin sensitization and atomization.The percentage of eosinophil （EOS） in the total number of white blood cells in the bronchoalveolar lavage fluid （BALF） was analyzed.The pathological changes of airway smooth muscle thickness were observed by HE staining in lung tissue sections.Western blot was used to detect the expression of phosphorylated p-JAK2 and p-STAT5 in lung tissue.Results The percentage of EOS in asthmatic model mice was shown to decrease significantly with glucocorticoid treatment （P〈0.05）.The thickness of airway smooth muscle in mice with glucocorticoid group was significantly lower than that in model group （P〈0.05）.The expression levels of p-JAK2 and p-STAT5 proteins were significantly reduced with glucocorticoids treatment （P〈0.05）.Conclusion Glucocorticoid can effectively relieve the proliferation of airway remodeling airway smooth muscle cells by regulating JAK2/STAT5 signaling pathway, which has a certain role in airway protection.