摘要
目的观察凋亡相关蛋白Bax与Bcl-2在吸烟伴慢性阻塞性肺疾病(COPD)患者与吸烟无COPD者肺组织中表达的差异性,探讨其在COPD发病中的作用。方法收集因肺部阴影行肺叶切除手术患者肺组织32例,其中吸烟伴COPD患者(A组)11例,吸烟无COPD者(B组)10例,不吸烟无COPD者(C组)11例,用免疫组化法(SP法)检测肺组织中Bax与Bcl-2蛋白的表达。结果 A组和B组肺泡间隔细胞中的Bax与Bcl-2阳性率、Bax/Bcl-2比值均明显高于C组(均P<0.05),A组肺泡间隔细胞中的Bax/Bcl-2比值明显高于B组(P<0.05)。肺泡间隔细胞中Bax阳性率、Bax/Bcl-2比值均与气流受限的肺功能指标(FEV1%pred,FEV1/FVC%)呈负相关。A组肺泡腔内巨噬细胞Bax/Bcl-2比值明显低于C组(P<0.05)。结论 Bax和Bcl-2在肺泡间隔细胞和肺泡腔内巨噬细胞表达的变化可能参与COPD发病机制。
Objective To investigate the expression of apoptotic proteins Bax and Bcl-2 in lung parenchyma of chronic obstructive pulmonary disease（COPD）patients and to explore the relationship between Bax/Bcl-2 ratio and COPD.Methods Surgically resected specimens from 11 smokers with COPD,10 smokers and 11 nonsmokers with normal lung function were analyzed.Markers of apoptosis including Bax and Bcl-2 proteins were detected by immunohistochemistry in both alveolar macrophages and alveolar walls.Results The Bax/Bcl-2 ratio was significantly higher in the pulmonary alveolar walls of smokers with COPD（P0.05）,and it was inversely correlated with lung function.On the contrary,the Bax/Bcl-2 ratio in alveolar macrophages was significantly lower in smokers with COPD than in nonsmokers without COPD（P0.05）,which may be one of the mechanisms contributing to less apoptosis of macrophages in COPD.Conclusion The changes of the Bax and Bcl-2 protein levels in the alveolar walls and macrophages may be involved in the pathogenesis of COPD.
出处
《华中科技大学学报（医学版）》
CAS
CSCD
北大核心
2010年第6期762-765,共4页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
2007~2009年度卫生部部属(管)医院临床学科重点项目(No.2007-353)
