中文摘要：

目的探讨在香烟诱导气道上皮细胞黏蛋白MUC5AC表达过程中Src／JNK信号通路的作用。方法香烟抽提物预处理的人气道上皮A549细胞，分别以活性氧（ROS）清除剂DMTU、JNK特异性抑制剂SP600125及Src激酶抑制剂PP2干预。测定各组细胞中ROS的含量，采用RT—PCR、ELISA法观察细胞黏蛋白（MUC）5AC转录水平及培养上清液中MUC5AC蛋白水平的改变，以Western blot法检测细胞表皮生长因子受体（EGFR）的蛋白表达。结果细胞暴露于不同浓度的香烟抽提物中，ROS的量呈浓度递增；ROS清除剂DMTU显著降低香烟所致的Src磷酸化；Src特异性抑制剂PP2处理组中的JNK磷酸化水平与对照组比较有明显下降，MUC5AC的表达水平也明显降低；JNK特异性抑制剂SP600125组中MUC5AC的蛋白表达和基因转录水平较对照组均明显降低。结论ROS-Src—JNK信号通路可能参与A549上皮细胞中MUC5AC的表达调控。

英文摘要：

Objective To explore the role of ROS/Src/JNK signaling pathway in cigarette smoke extract（CSE）-induced mucin （MUC） SAC production in A549 airway epithelial cells. Methods The A549 airway epithelial cells were cultured in medium with CSE, then treated with ROS scavenger DMTU, c-Jun Nterminal kinase（JNK） specific inhibitor SP600125, and Src kinase inhibitor PP2, respectively. The relative content of reactive oxygen species （ROS） were assayed by special kit. The levels of MUCSAC in culture medium,epidermal growth factor receptor（ EGFR）, activated EGFR and MUCSAC mRNA in culture cells were detected with ELISA, Western Blot and RT-PCR,respectively. Results A dose-dependent increasing of ROS production in cells exposed to dilutions of cigarette smoke solution was detected. DMTU inhibited cigarette smoke-induced Src phosphorylation （ P 〈0. 05 ）. SP600125 reduced the expression of MUCSAC （ P 〈 0. 05 ） compared with the normal group. The activation of JNK was suppressed by Src specific inhibitor PP2 （P 〈 0.05 ）. Conclusion ROS/Src/JNK signal cascade may play a particular role in MUCSAC expression of A549 cells induced by cigarette smoke.