中文摘要：

背景：尽管支气管的平滑肌房间(BSMC ) 在航线在长期的气喘期间改变起一个关键作用，这被认出， BSMC 怎么施加他们的煽动性的功能，很好没被理解。表明小径的细胞外的调整信号的激酶 1/2 (ERK1/2 ) 是在长期的气喘，而是它对由 BSMC 的分泌物的影响的一条重要发信号小径一直不是学习得好的。我们调查了在这研究在长期的气喘的一个老鼠模型由 BSMC 在分泌物上表明小径的 ERK1/2 的影响。方法：为了创造长期的气喘的一个老鼠模型，， Wistar 老鼠经历了 ovalbumim (卵) 注射和八星期吸入。BSMC 被孤立并且有教养的在试管内。表皮的生长因素， PD98059 和 ERK1/2 反察觉到 oligonucleotide 被用来探索表明小径的 ERK1/2 的角色。在 BSMC 的 P-ERK1/2 (phospho-ERK1/2 ) 的表示被西方的污点和反向的 transcriptase 聚合酶链反应(RT-PCR ) 分析。BSMC 的分泌物被连接酶的免疫吸着剂试金(ELISA ) 检测。结果：Phospho-ERK1/2 表示与控制相比在长期的气喘的老鼠的 BSMC 被增加。PD98059 禁止了 phospho-ERK1/2 蛋白质的表示，当有反感觉 oligonucleotide 的处理禁止了 P-ERK1/2 mRNA 和蛋白质的表示时。从长期的气喘组获得的 BSMC 分泌了生长因素的显著地更大的数量(转变生长因素( TGF )-beta(1),脉管的内皮生长因素( VEGF )和结缔组织生长因素( CTGF ))， cytokines (在激活之上调整了，表示房间、藏匿的正常 T ( RANTES )和 eotaxin )，并且细胞外的矩阵( fibronectin 和骨胶原我)与正常控制相比。在长期的气喘的组，而是反应的刺激分泌物组织的表皮的生长因素是更强烈的。PD98059 和反感觉 oligonucleotide 在长期的 ashmatic 老鼠由 BSMC 压制了分泌物。Antisense oligonucleotide 将近把 RANTES 的水平归结为正常控制的，当 PD98059 不能时。结论：这些结果建议 ERK1/2 发信号小径可以在长期的气喘的老鼠在 BSMC 的扩充分泌物起一个重?

英文摘要：

Background Although it is recognized that bronchial smooth muscle cells （BSMCs） play a key role. in airway remodeling during chronic asthma, it is not well understood how BSMCs exert their inflammatory functions. The extracellular signal-regulated kinase 1/2 （ERK1/2） signaling pathway is an important signaling pathway in chronic asthma but its influence on secretion by BSMCs has not been well-studied. We investigated the impact of ERK1/2 signaling pathway on secretion by BSMCs in a rat model of chronic asthma in this study. Methods To create a rat model of chronic asthma, Wistar rats underwent ovalbumim （OVA） injection and eight weeks of inhalation. BSMCs were isolated and cultured in vitro. Epidermal growth factor, PD98059 and ERK1/2 antisense oligonucleotide were used to explore the role of ERK1/2 signaling pathway. The expression of P-ERK1/2 （phospho-ERK1/2） in BSMCs was analyzed by Western blot and reverse transcriptase-polymerase chain reaction （RT-PCR）. Secretion of BSMCs was detected by enzyme-linked immunosorbent assay （ELISA）. Results Phospho-ERK1/2 expression was increased in BSMCs of chronic asthmatic rats compared with the controls. PD98059 inhibited expression of phospho-ERK1/2 protein, while treatment with an antisense oligonucleotide inhibited the expression of P-ERK1/2 mRNA and protein. BSMCs obtained from the chronic asthma group secreted significantly greater quantities of growth factors （transforming growth factor （TGF）-β1, vascular endothelial growth factor （VEGF） and connective tissue growth factor （CTGF））, cytokines （regulated upon activation, normal T cell-expressed and secreted （RANTES） and eotaxin）, and extracellular matrix （fibronectin and collagen I） compared with normal controls. Epidermal growth factor stimulated secretion in both groups, but the response of the chronic asthma group was more intense. Both PD98059 and antisense oligonucleotide suppressed secretion by BSMCs in chronic ashmatic rats. Antisense oligonucleotide reduced t