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AP-2α expression and cell apoptosis of the lung tissue of rats with COPD and ECV304 cells stimulated by cigarette smoke extract

AP-2α expression and cell apoptosis of the lung tissue of rats with COPD and ECV304 cells stimulated by cigarette smoke extract

作     者:LI JunLi CHEN Yan CHEN Ping CAI Shan PENG Hong ZHOU Rui XIANG XuDong LONG Hong LIU ShaoKun 

作者机构:Department of Respiratory Medicine Xiangya Second Hospital of Central South University Changsha Hunan 410011 China 

出 版 物:《Chinese Science Bulletin》 (中国科学通报)

年 卷 期:2011年第56卷第15期

页      面:1562-1568页

核心收录:

学科分类:1002[医学-临床医学] 100201[医学-内科学(含:心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基  金:supported in part by the National Natural Science Foundation of China (30770931 81070039) 

主  题:慢性阻塞性肺病 细胞凋亡 香烟烟雾 提取物 AP 大鼠 caspase 癌组织 

摘      要:An increasing body of evidence suggests that apoptosis of structural cells in the lung might be an important upstream event in the pathogenesis of chronic obstructive pulmonary disease (COPD).AP-2α is one of the important transcription factors involved in the modulation of apoptosis in carcinogenesis and idiopathic-dilated *** relationship between AP-2α and apoptosis in COPD remains to be *** aim of the present study was to investigate the expression of AP-2α in the lung tissues of rats with COPD induced by smoking and its possible protective effect on cigarette smoke extract (CSE) induced endothelial cell ***-Dawley rats (n=24) were randomly assigned to normal and COPD *** COPD group was exposed to smoke from 20 commercial unfiltered cigarettes for 80 d before morphological assessment of the lung tissue was *** expression of AP-2α in lung tissues was measured by Western *** demonstrate the relationship between apoptosis and AP-2α,in vitro cell experiments were carried *** were treated with different concentrations of CSE before proliferation was measured by *** was then determined by Hoechst staining and the expression of cleaved caspase-3 and AP-2α by Western blotting over time following treatment with 5% *** were then infected with an AP-2α adenovirus vector and the expression of cleaved caspase-3 and AP-2α was compared to the control groups by Western *** COPD group showed larger air spaces and significant decrease of FEV 0.3/FVC compared with the rats in the control group (P0.05).The expression of AP-2α was significantly higher in the lung tissue of rats with COPD compared with those of controls (P0.05).In the ECV304 cells,CSE induced apoptosis (P0.01) and caspase-3 activation in a time-dependent manner and reduced the cell proliferation rate in a dose-dependent manner (P0.005).Moreover,5% CSE treatment increased endogenous AP-2α protein ***-2α overexpr

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