中文摘要：

目的：研究白介素13（Interleukin-13,IL-13）对气道上皮细胞粘液分泌的效应并探讨其作用机制。方法：HBE16细胞在无血清培养基中培养24小时后加入IL-13刺激24小时,ELISA检测粘蛋白（MUC）5AC的表达;Western检测磷酸化细胞外信号调节激酶1/2（Extracellular signal-regulated kinase 1/2,ERK1/2）和磷酸化c-Jun氨基端激酶1/2（c-Jun N-terminal kinase 1/2,JNK1/2的表达;使用SP600125阻滞JNK信号通路后检测MUC5AC蛋白表达;RT-PCR检测STAT4和STAT6的表达变化;EMSA检测通路下游核蛋白FOXA2的表达。结果：IL-13刺激24小时后MUC5AC和p-JNK1/2表达升高,而p-ERK1/2表达无显著变化;使用SP600125阻断JNK通路表达后,MUC5AC表达减弱;IL-13刺激后STAT4表达无显著变化,STAT6表达显著升高,FOXA2表达显著降低。结论：IL-13通过JNK-STAT6-FOXA2通路调控粘液分泌。

英文摘要：

Objective：To investigate the effect of interleukin-13（IL-13） on mucus secretion in vitro and the possible mechanism.Methods：HBE16 cells were serum-starved for 24 h and exposed to IL-13 for 24 h.The level of MUC5AC was detected using ELISA.The phosphorylation of extracellular signal-regulated kinase 1/2（ERK1/2） and c-Jun N-terminal kinase 1/2（JNK1/2） were also examined also.The cells were pretreated with SP600125 for 1 h and then the level of MUC5AC was measured.RT-PCR was performed to examine the mRNA level of STAT4 and STAT6.Electrophoretic mobility shift assays （EMSA） were performed to examine the DNA-binding activity of Forkhead box a2（FOXA2）.Results：IL-13 caused a significant increase of MUC5AC and p-JNK1/2,yet failed to affect the phosphorylation of ERK1/2.The expression of MUC5AC was attenuated after treatment with SP600125.A significant increase in STAT6 was observed in IL-13 group compared to that of the saline-treatment group,whereas the expression of STAT4 was not significantly affected.The DNA-binding activity of FOXA2 was down-regulated after exposed to IL-13.Conclusion：Our study suggestes that IL-13 down-regulates mucus secretion via JNK-STAT6FOXA2 pathway in vitro.