摘要目的 探讨吸烟对支气管哮喘(简称哮喘)大鼠气道壁厚度及转化生长因子β1 mRNA(TGF-β1 mRNA)和Ⅲ型胶原表达的影响及作用机制.方法 健康雄性Wistar大鼠30只,按随机数字表法分为对照组、哮喘组和吸烟组,每组10只.用卵白蛋白致敏并吸入激发制备哮喘模型.吸烟组定量吸入香烟烟雾.采用逆转录-聚合酶链反应(RT-PCR)法测量TGF-β1 mRNA和免疫组化法测量Ⅲ型胶原表达.采用SPSS 11.0软件,所有数据以-x±s表示,组间比较采用单因素方差分析,组间差异比较采用LSD方差分析法,采用Pearson相关分析.结果 (1)吸烟组TGF-β1 mRNA、Ⅲ型胶原表达的吸光度(A)值分别为0.42±0.04、25.8±2.3,哮喘组分别为0.39±0.04、22.9±3.1,对照组分别为0.26±0.04、16.3±2.3,3组间比较差异有统计学意义(F值分别为55.97,35.61,P均＜0.05);(2)Pearson相关分析结果表明TGF-β1 mRNA与Ⅲ型胶原的表达呈正相关(r=0.71,P＜0.05);(3)气道壁厚度吸烟组为(23.3±2.4)μm2/μm,哮喘组为(20.1±2.9)μm2/μm,对照组为(11.6±2.4)μm2/μm,3组间比较差异有统计学意义(F=53.68,P＜0.05).结论 吸烟通过促进哮喘大鼠气道TGF-β1 mRNA的过度表达,增加气道Ⅲ型胶原表达,加重气道重塑的发生.

abstractsObjective To study the effect of cigarette smoke on the expression of transforming growth factor-beta 1(TGF-β1),and collagen type Ⅲ in lung tissues,and therefore to investigate the mechanism of airway remodeling. Methods 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-β1 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 -x±s). Group comparison was made by one way ANOVA and Pearson correlation was used for correlation analysis. Results The levels of TGF-β1 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-β1 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)μm2/μm was significantly higher than that in the asthmatic group(20.1±2.9)μm2/μm and the control group(11.6±2.4) μm2/μm;compared to the control group,it was higher in the asthmatic group (F=53.68,P＜0.05). Conclusion Cigarette smoke can promote over-expression of TGF-β1-mRNA in asthmatic rat airways, increase the expression of collagen type Ⅲ and aggravate airway remodeling.