α_1-AR通过ERK途径诱导人胚肺成纤维细胞增殖  

α_1-AR induced proliferation on human embryo fibroblasts via an ERK pathway

作　　者：康小文[1] 蒋哲[1] 吴开明[2] 吴晓梅[1] 李兆国[1] 

机构地区：[1]哈尔滨医科大学附属二院呼吸科,黑龙江哈尔滨150086 [2]黑龙江中医药大学附属第一医院甲状腺科,黑龙江哈尔滨150086

出　　处：《临床肺科杂志》2015年第8期1359-1361,1364,共4页Journal of Clinical Pulmonary Medicine

基　　金：黑龙江省教育厅科研课题(No 12541563)

摘　　要：目的探讨α1-AR对人胚肺成纤维细胞增殖的影响及其机制。方法体外培养HFL-1,分为以下4组:(1)空白对照组(control组);为单纯HFL-1培养;(2)α1-AR激活组(PE组);(3)α1-AR抑制组(Pra组);(4)PD98059组。MTT法药物毒性分析;Brd U法检测细胞增殖;蛋白质印迹(western blot)检测ERK活性检测。结果 MTT法结果显示PE10μM组细胞活力最佳;Brd U法检测结果显示PE诱导细胞增殖与浓度和时间相关。western blot结果显示:PE能够诱导ERK磷酸化,在作用10 min时达到最大状态。结论α1-AR激活诱导ERK磷酸化从而促进人胚肺成纤维细胞增殖。Objective To investigate the effect of α1-AR activation on the proliferation of human embryo fi-broblasts and the potential mechanism. Methods HFL-I were cultured in vitro and divided into 4 groups： the con-trol group, the PE group, the Pra group, and the PD98059 group. Drug toxicity was analyzed by MTT, cellular pro-liferation was detected by BrdU, and ERK activity was detected by western blot. Results MTF assay indicated that cells had best vitality in the PE10 μM group. BrdU results showed that PE-induced proliferation was correlated with concentration and time. Western blot demonstrated that PE induced phosphorylation of ERK and peaked at 10 min. Conclusion α1-AR induces phosphorylation of ERK, which further promotes cellular proliferation in human embryo fibroblasts.

关 键 词：肺成纤维细胞 肾上腺素受体 增殖 肺纤维化 

分 类 号：R563.9[医药卫生—呼吸系统]