雌激素对香烟烟雾诱导肺上皮间质转化的影响  

Effect of estrogen on cigarette smoke-induced pulmonary epithelial mesenchymal transformation

作　　者：杨晓蕾[1] 李娜[1] 范敏娟[1] 张金桃 刘向 YANG Xiaolei;LI Na;FAN Minjuan;ZHANG Jintao;LIU Xiang(Department of General Practice,the Second Affiliated Hospital of Kunming Medical University,Kunming 650101,China)

机构地区：[1]昆明医科大学第二附属医院全科医学科,昆明650101

出　　处：《实用医学杂志》2022年第2期150-155,共6页The Journal of Practical Medicine

基　　金：云南省科技厅-昆明医科大学应用基础研究联合专项资金项目[编号:2018FE001(-45)]。

摘　　要：目的探究在慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)中,雌激素通过调控miR-21/SMAD信号通路对香烟烟雾诱导的肺上皮间质转化(epithelial mesenchymal transition,EMT)的影响。方法 RT-qPCR、Western blot、MTT检测miR-21及E-cadherin、α-SMA、Vimentin mRNA水平、SMAD相关蛋白表达、HBE增殖活力。结果雌激素促进香烟烟雾(CSE)诱导的人肺支气管上皮细胞(HBE)EMT和活力下降;上调miR-21,激活SMAD通路;促进CSE诱导的EMT和细胞活力下降;过表达miR-21,激活SMAD通路;雌激素通过激活SMAD促进CSE诱导的EMT和细胞活力下降。结论雌激素通过上调miR-21,激活SMDA通路,抑制HBE增殖,促进HBE发生EMT,促进COPD发展进程。Objective To explore the effect of estrogen on cigarette smoke-induced epithelial mesenchymal transition(EMT)in chronic obstructive pulmonary disease(COPD)patients by regulating miR-21/SMAD signaling pathway. Methods The mRNA levels of miR-21,E-cadherin,α-SMA and vimentin,the expression of SMADrelated proteins and the proliferation activity of HBE were detected by RT-qPCR,Western blot and MTT. Results Estrogen promoted the decrease of EMT and vitality of HBE cells induced by CSE,up-regulated miR-21 to activate SMAD pathway,promoted the decline of EMT and cell vitality induced by CSE;It activated SMAD pathway by overexpressing miR-21. It could promote the declines of CSE-induced EMT and cell viability by activating SMAD.Conclusion Estrogen can activate SMDA pathway by up-regulating miR-21 and promote COPD development by inhibiting HBE proliferation and promoting its EMT.

关 键 词：雌激素 MIR-21 SMAD 慢性阻塞性肺疾病 上皮间质转化 

分 类 号：R563[医药卫生—呼吸系统]