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目的 探讨吸烟时转化生长因子 β1 (TGF β1 )在吸烟引起的慢性支气管炎与肺气肿中的作用。方法 建立吸烟时引起的慢性支气管炎与肺气肿的动物模型 ,2 0只雄性叙利亚金黄地鼠分为正常组和吸烟组 ,每组各 1 0只 ;体外培养支气管上皮细胞并经香烟烟雾提取物 (CSE)刺激。观察肺内和支气管上皮细胞TGF β1 mRNA和蛋白表达情况。结果 吸烟组于 3个月时出现慢性支气管炎和肺气肿的病理改变 ,免疫组化结果显示 ,吸烟组TGF β1 的阳性强度 (2 .75± 0 2 3)与正常组 (0 .84± 0 39)比较差异有显著性 (P =0 .0 0 1 )。两组的TGF β1 mRNA吸光度分别为 1 .2 8和 0 .98。支气管上皮在CSE刺激后 ,细胞形态发生明显变化 ,TGF β1 的表达增强 ,与单纯培养组比较差异有显著性 (2 .67± 0 1 6vs0 .85± 0 54 ,P =0 .0 0 1 )。结论 烟雾刺激造成气道上皮的损伤 ,产生大量的TGF β1 ,该变化可能是吸烟引起慢性支气管炎和肺气肿的机制之一
Objective To investigate the role of transforming growth factor-β1 (TGF-β1) in smoking-induced chronic bronchitis and emphysema during smoking. Methods Animal models of chronic bronchitis and emphysema caused by smoking were established. Twenty male Syrian hamsters were divided into normal group and smoking group, with 10 rats in each group. Bronchial epithelial cells were cultured in vitro and extracted by cigarette smoke (CSE) stimulation. The expression of TGFβ1 mRNA and protein in lung and bronchial epithelial cells was observed. Results The pathological changes of chronic bronchitis and emphysema were found in the smoking group at 3 months. The results of immunohistochemistry showed that the positive expression of TGF β1 (2.75 ± 0.23) in the smoking group was significantly lower than that in the normal group (0.84 ± 0 39) the difference was significant (P = 0.010). The TGFβ1 mRNA absorbance in both groups was 1.28 and 0.98, respectively. After CSE stimulation, the morphology of bronchial epithelial cells changed significantly, and the expression of TGFβ1 was enhanced, which was significantly different from that of pure culture group (2.67 ± 0.16 vs0.85 ± 54.0, P = 0.001) . Conclusion Smog stimulation can damage airway epithelium and produce a large amount of TGFβ1, which may be one of the mechanisms of smoking causing chronic bronchitis and emphysema