COPD模型大鼠肺组织TGF-β1 mRNA的表达及意义

Significance and expression of TGF-β1 mRNA Expression in lung tissue of COPD model rats

目的探讨转化生长因子良（TGF-β1）在长期吸烟所致慢性阻塞性肺疾病（COPD）病理变化中的作用。方法将大鼠随机分为对照组和模型组，分别分为1-6月组，每组6只。建立大鼠吸烟COPD模型。光镜下观察吸烟对大鼠肺组织结构的影响，RT-PCR方法检测TGF-β1mRNA在肺组织中的表达。结果随吸烟时间延长，肺泡腔不规则扩大，肺泡间隔破裂，有的肺泡融合成肺大泡，以吸烟6月组最为明显，肺组织结构表明COPD模型建立成功。RT-PCR结果表明，TGF-β1mRNA在正常肺组织中呈微弱表达，随吸烟时间的延长，TGF-β1mRNA表达增多，5月组表达最多。结论长期吸烟可引起气道壁炎细胞浸润及肺组织形态学变化，导致COPD发生。TGF-β1，表达随吸烟月份增加逐渐增多，肺组织结构破坏与TGF-β1表达有相关性，表明TGF-β1在COPD的发生和发展过程中起重要作用。

Objective To investigate the role of TGF-β1 on pathological changes of long -term smoklng-induced chronic obstructive pulmonary disease （COPD）. Methods Wistar rats were divided into the control group and the smoking group at random. The two groups were divided into one to six month group individually and there was six rats in each group. The smoking COPD model of Wistar rats was established. The influence of smoking on lung tisse structure of rats were ob- served by light microscope. The expressions of TGF-β1 mRNA in lung tissues were detected by trans-reverse polymerase chain reaction （RT-PCR）. Results Along with the extended smoking time, the cavity of alveolus expanded anomally, the alveolus interval broked and some alveolus was mixed together to form pneumatocele. It was the most conspicuous for the sixth months smoking group. Lung tissue structure showed that the model of COPD was established succeedly. The results of RT-PCR Showed that the expressions of TGF-β1 mRNA in normal lung tissues were faint, along with the lengthened smoking times, the expressions of TGF-β1 mRNA increased, it was the most conspicuous in the fifth month. Conclusions Long-term smoking may result in the infiltration of inflammatory cells in the bronchiolar walls and the morphology changes of lung tissues, leading to COPD. Along with the adding smoking months, the expressions of TGF-β1mRNA increase. The damage of lung tissue may correlate with the expressions of TGF-β1mRNA, It indicates that TGF-β1may act an important function on generation and development in COPD.