AP-2α在烟雾暴露所致慢性阻塞性肺疾病大鼠肺组织中的表达及与肺间隔细胞凋亡的关系

Expression of AP-2α in lung tissue of passive-smoking rats and its correlation with apoptosis of alveolar septal cells

目的探讨熏烟所致慢性阻塞性肺疾病（chronic obstructive pulmonary disease，COPD）大鼠肺组织中AP-2α表达与肺间隔细胞凋亡的关系。方法采用被动吸烟80d来复制大鼠COPD模型，采用TUNEL法检测肺组织细胞凋亡、Western blot法检测肺组织中活化的半胱天冬酶类3（Caspase-3）、免疫组织化学及Western blot法检测胞核中AP-2α蛋白的表达。结果采用熏烟法成功复制了大鼠COPD模型。与对照组相比，COPD组大鼠肺组织中活化的Caspase-3增加，肺间隔细胞凋亡增多；肺组织中AP-2α的阳性率增加，胞核中AP-2α蛋白水平增加（P〈0．05）。结论AP-2α可能参与了烟雾暴露所致的大鼠肺间隔细胞凋亡及COPD的发生。

Objective To investigate the relationship between the apoptosis of alveolar septal cells and the expression of AP-2α in lung tissue of rats with chronic obstructive pulmonary disease（COPD）. Methods Rat models of COPD were replicated by passive smoking for 80 days. The alveolar septal cells apoptosis were detected by using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） methods and active caspase-3 in the lung tissue was measured by Western blot. The expression of AP-2α in rat lung tissue was detected by immunohistochemistry and Western blot. Results Rat models of COPD were replicated successfully by passive smoking. Compared with those of normal group, the apoptosis rate of alveolar septal cells and the expression of active caspase-3 in the lung tissue were increased in COPD group. The expression of AP-2α was significantly higher than that from the controls （ P 〈0.05）. Conclusions AP-2α may contribute to the pathogenesis of smoking-rat COPD and affect the apoptosis of alveolar septal cells.