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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β_1(TGF-β_1)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-β_1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-β_1、Smad4、SLPI的表达,用逆转录聚合酶链法检测支气管肺组织中 TGF-β_1、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-β_1阳性系数(3.91)、TGF-β_1 mRNA 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-β_1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-β_1表达增加所致,其机制可能通过 Smads 信号转导通路介导。
Objective To investigate the expression of secreted leukocyte protease inhibitor (SLPI) in bronchial and lung tissues of chronic obstructive pulmonary disease (COPD) rats and the effect of transforming growth factor β 1 (TGF-β 1). Methods The model of COPD was induced by injecting lipopolysaccharide (LPS) with smoked cigarettes, and the lung function and pathological changes of rats were detected by the intervention of TGF-β1 monoclonal antibody. The levels of IL-6 and IL-6 in bronchoalveolar lavage fluid The expression of TGF-β_1, Smad4 and SLPI in bronchial lung tissue was detected by immunohistochemical method. The expression of TGF-β_1, Smad4 and SLPI mRNA in bronchial lung tissue was detected by reverse transcription-polymerase chain reaction. Measurement data were compared using one-way analysis of variance, multiple comparison of two sample means using t test, rank data using non-parametric test of rank conversion. Results The SLPI positive rate (1.07), the SLPI mRNA absorbance (0.17 ± 0.01) and the SLPI concentration in BALF [(47 ± 4) μg / L] in model group were significantly higher than those in normal control group [ 0.10, and 82 ± 7 μg / L, respectively). The positive rate of TGF-β 1 (3.91) and TGF-β 1 mRNA (0.71 ± 0.09) )] Was significantly higher. After intervention with TGF-β 1, the SLPI positive coefficient (SLR), the SLPI mRNA absorbance (0.59 ± 0.05) and the SLPI concentration in BALF [(69 ± 6) μg / L] (1.07), (0.17 ± 0.01) and (47 ± 4) μg / L]. Expiratory peak flow [(28 ± 6) ml / s], forced expiratory volume at 0.3 second (4.4 ± 1.3) ml and forced expiratory volume at 0.3 second (80 ± 10)% The model group rats [(23 ± 5) ml / s, (3.3 ± 1.4) ml and (62 ± 9)%] were significantly improved. Conclusion The SLPI in bronchopulmonary tissues of COPD rats is significantly decreased, which may be due to the increased expression of TGF-β 1. The mechanism may be mediated through the Smads signal transduction pathway.