@Article {Milara1264，作者= {Milara，Javier和Serrano，Adela和Peir {\'o}，Teresa和Artigues，Enrique和Gavald {\ a a}，Amadeu和Miralpeix，Montse和Morcillo，Esteban J.和Esteban J.和Cortban J.和Cortban J.和Cortban J.Julio}，title = {aclidinium抑制香烟烟雾诱导的肺成纤维细胞至元素纤维细胞过渡}，音量= {41}，number = {6}，pages = {1264---1274}，ear{10.1183/09031936.00017712}，出版商= {欧洲呼吸社会}，188bet官网地址摘要= {香烟吸烟有助于慢性阻塞性肺部疾病（COPD）的肺重塑。作为此次重塑的一部分，在COPD患者的小气道中观察到周环纤维化，并导致气道阻塞。成纤维细胞到肌纤维细胞过渡是周围纤维化形成的关键步骤。这项体外研究检查了香烟烟雾对支气管成纤维细胞到肌纤维细胞过渡的影响，以及溴化烷基溴化物是否抑制了这一过程。将人支气管成纤维细胞与溴化烷基（10-9 {\ textendash} 10-7 m）一起孵育，并暴露于香烟烟雾提取物中。I型I型胶原蛋白和α-平滑肌肌动蛋白（α-SMA）表达通过实时PCR和Western印迹作为肌纤维细胞标记来测量。细胞内活性氧，环状AMP（CAMP），细胞外信号调节激酶（ERK）1/2和胆碱乙酰转移酶作为细胞内信号传导介质测量。烟雾诱导的I型胶原蛋白和α-SMA是由活性氧，细胞内cAMP的耗竭以及ERK1/2磷酸化和胆碱乙酰基转移酶的增加来介导的。 These effects could be reversed by treatment with the anticholinergic aclidinium bromide, by silencing the mRNA of muscarinic receptors M1, M2 or M3, or by the depletion of extracellular acetylcholine by treatment with acetylcholinesterase. A non-neuronal cholinergic system is implicated in cigarette smoke-induced bronchial fibroblast-to-myofibroblast transition, which is inhibited by aclidinium bromide.}, issn = {0903-1936}, URL = {//www.qdcxjkg.com/content/41/6/1264}, eprint = {//www.qdcxjkg.com/content/41/6/1264.full.pdf}, journal = {European Respiratory Journal} }