Expression of secretory leukocyte proteinase inhibitor in the bronchi and lung tissues of chronic obstructive pulmonary disease rat models and the regulatory mechanism by transforming growth factor β1
- Author:
- No author available
- Journal Title:
- CHINESE JOURNAL OF TUBERCULOSIS AND RESPIRATORY DISEASES
- Issue:
- 11
- DOI:
- 10.3760/j.issn:1001-0939.2007.11.013
- Key Word:
- 肺疾病,阻塞性;转化生长因子β
Abstract： 目的 探讨分泌性白细胞蛋白酶抑制物(SLPI)在慢性阻塞性肺疾病(COPD)大鼠支气管肺组织中的表达及转化生长因子β1(TGF-β1)的影响.方法 采用熏香烟加气管内注射脂多糖复制大鼠COPD模型,并用TGF-β1单抗干预,测定大鼠的肺功能及病理变化结果,应用酶联免疫法检测支气管肺泡灌洗液(BALF)中SLPI水平,用免疫组织化学法观察支气管肺组织TGF-β1、Smad4、SLPI的表达,用逆转录聚合酶链法检测支气管肺组织中TGF-β1、Smad4和SLPI mRNA的表达.计量资料比较采用单因素方差分析,两样本均数的多重比较采用t检验,等级资料采用秩转换的非参数检验.结果 模型组大鼠SLPI阳性系数(1.07)、SLPI mRNA吸光度值(0.17±0.01)和BALF中SLPI浓度[(47±4)μg/L]比正常对照组大鼠[(3.86)、(0.84±0.10)和(82±7)μg/L]明显降低;TGF-β1阳性系数(3.91)、TGF-β1mRNA吸光度值(0.71±0.09)比正常对照组大鼠[(1.12)、(0.15±0.01)]显著增高.经TGF-β1单抗干预后,干预组大鼠SLPI阳性系数(2.69)、SLPI mRNA吸光度值(0.59±0.05)和BALF中SLPI浓度[(69±6)μg/L]比模型组大鼠[(1.07)、(0.17±0.01)和(47±4)μg/L]有明显提高.呼气峰流量[(28±6)ml/s]、第0.3秒用力呼气容积[(4.4±1.3)ml]和第0.3秒用力呼气容积/用力肺活量[(80±10)%]比模型组大鼠[(23±5)ml/s、(3.3±1.4)ml和(62±9)%]有显著改善.结论 COPD大鼠支气管肺组织中SLPI明显减少,可能是TGF-β1表达增加所致,其机制可能通过Smads信号转导通路介导.
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