虫草素抑制脂多糖诱导的支气管上皮细胞炎症反应

Cordycepin suppresses lipopolysaccharide-induced inflammatory responses in human bronchial epithelial cells

目的:探究虫草素对支气管上皮细胞炎症反应的调节作用及其机制。方法:培养人支气管上皮细胞系(16HBE),选择状态良好的16HBE细胞分别用不同浓度的虫草素(0、10、20、40、60μmol/m L)处理4 h后,脂多糖(1mg/L)处理12 h,MTT法检测细胞存活力;采用荧光定量PCR检测炎症细胞因子IL-8、TNF-α的mRNA相对表达水平;蛋白质印迹法检测p-AKT2、AKT2的蛋白表达水平。结果:虫草素能以剂量依赖的方式提高细胞存活力(P<0.05),抑制脂多糖诱导的IL-8、TNF-α的mRNA相对表达量(P<0.05),减少脂多糖活化的p-AKT2水平(P<0.05)。结论:虫草素在减弱脂多糖诱导的支气管上皮细胞炎症反应中起重要作用,其机制可能涉及AKT2信号通路的下调。

Objective：To investigate the role of cordycepin in regulating the inflammatory response of human bronchial epithelial cells and its underlying mechanism.Methods：The human bronchial epithelial cells（16HBE）,which grew in good condition,were treated with different concentrations of cordycepin（0,10,20,40,60 μmol/m L） for 4 hours and then treated with lipopolysaccharide（LPS,1 mg/L） for 12 hours.MTT assay was used for the detection of cell vitality.At the same time,the mRNA expression level of inflammatory cytokines（IL-8,TNF-α） was evaluated by quantitative real-time PCR.The level of pAKT2 expression was analyzed by Western blotting analysis.Results：Cordycepin could protect bronchial epithelial cells from damage of LPS in a concentration-dependent manner（P 0.05）,and attenuated LPSinduced release of pro-inflammatory cytokines（P 0.05）,down-regulate the phosphorylation level of AKT2 induced by LPS（P 0.05）.Conclusion：Cordycepin shows active inhibitory effect on the inflammatory response of 16 HBE cells,possibly through mediating relevant signal pathway of AKT2.