Guo Zhi-hong, DU Yong-cheng, Xu Jian-ying
Department of Respiratory Medicine, The First Hospital of Shanxi Medical University, Taiyuan 030001, China.
Zhonghua Jie He He Hu Xi Za Zhi. 2008 Jan;31(1):42-5.
To study the effect of cigarette smoke on the expression of transforming growth factor-beta l (TGF-beta1), and collagen type III in lung tissues, and therefore to investigate the mechanism of airway remodeling.
Thirty male Wistar rats were randomly divided into a control group, an asthmatic group and a cigarette smoke treated group, with 10 rats in each group. The expression level of TGF-beta1 mRNA was measured by reverse transcription polymerase chain reaction (RT-PCR) and collagen type III by immunohistochemistry. The thickness of airway wall in each group was also measured. Software SPSS 11.0 was used for statistical analysis (data expressed as +/- s). Group comparison was made by one way ANOVA and Pearson correlation was used for correlation analysis.
The levels of TGF-beta1 mRNA and collagen type III in cigarette smoke treated group (0.42 +/- 0.04, 25.8 +/- 2.3) were higher than those in the asthmatic group (0.39 +/- 0.04, 22.9 +/- 3.1) and in the control group (0.26 +/- 0.04, 16.3 +/- 2.3). Compared to the control group, the levels were higher in the asthmatic group (F = 55.97, 35.61, all P < 0.05). The level of TGF-beta1 mRNA was positively correlated with the expression of collagen type III (r = 0.71, P < 0.05). The thickness of airway wall in the cigarette smoke treated group (23.3 +/- 2.4) microm2/microm was significantly higher than that in the asthmatic group (20.1 +/- 2.9) microm2/microm and the control group (11.6 +/- 2.4) microm2/microm;compared to the control group, it was higher in the asthmatic group (F = 53.68, P < 0.05).
Cigarette smoke can promote over-expression of TGF-beta1-mRNA in asthmatic rat airways, increase the expression of collagen type III and aggravate airway remodeling.
研究香烟烟雾对肺组织中转化生长因子-β1（TGF-β1）及Ⅲ型胶原蛋白表达的影响，进而探讨气道重塑的机制。
将30只雄性Wistar大鼠随机分为对照组、哮喘组和香烟烟雾处理组，每组10只。采用逆转录聚合酶链反应（RT-PCR）检测TGF-β1 mRNA的表达水平，免疫组织化学法检测Ⅲ型胶原蛋白的表达。同时测量每组气道壁厚度。使用SPSS 11.0软件进行统计分析（数据以±s表示）。组间比较采用单因素方差分析，Pearson相关分析用于相关性分析。
香烟烟雾处理组TGF-β1 mRNA和Ⅲ型胶原蛋白水平（0.42±0.04，25.8±2.3）高于哮喘组（0.39±0.04，22.9±3.1）和对照组（0.26±0.04，16.3±2.3）。与对照组相比，哮喘组上述水平也较高（F=55.97，35.61，均P<0.05）。TGF-β1 mRNA水平与Ⅲ型胶原蛋白表达呈正相关（r=0.71，P<0.05）。香烟烟雾处理组气道壁厚度（23.3±2.4）μm²/μm显著高于哮喘组（20.1±2.9）μm²/μm和对照组（11.6±2.4）μm²/μm；与对照组相比，哮喘组气道壁厚度也较高（F=53.68，P<0.05）。
香烟烟雾可促进哮喘大鼠气道TGF-β1-mRNA的过度表达，增加Ⅲ型胶原蛋白的表达，加重气道重塑。
