持续气道正压通气对慢性阻塞性肺病大鼠支气管肺组织的保护作用

Protective effects of continuous positive airway pressure against bronchopulmonary tissue of chronic obstructive pulmonary disease rat

目的探讨持续气道正压通气(CPAP)产生的外源扩张性压力对于慢性阻塞性肺病(COPD)大鼠肺组织的保护作用。方法将40只Wistar大鼠随机分为4组,每组10只,分别为正常对照组、假手术组、COPD模型组和COPD造模后进行CPAP治疗组。采用烟雾吸入法制作大鼠COPD模型。采用HE染色观察各组大鼠的肺组织病理学改变;免疫组织化学法检测磷酸化表皮生长因子(p-EGFR)、磷酸化细胞外信号调节激酶(p-ERK)和转化生长因子β1(TGF-β1)蛋白的表达水平;RT-PCR检测EGFR和TGF-β1mRNA的相对表达量;Western blotting检测p-EGFR、ERK、p-ERK和TGF-β1蛋白的相对表达量。结果与正常对照组比较,COPD模型组大鼠的支气管肺组织病理改变明显,EGFR、ERK、TGF-β1的表达水平及磷酸化程度均显著增强(P<0.01);经CPAP治疗后,上述指标相对模型组均显著下调(P<0.01);但假手术组与正常对照组比较差异无统计学意义(P>0.05)。结论 CPAP治疗对COPD大鼠肺组织炎症的改善可能与EGFR和TGF-β信号通路的调节有关。

Objective To explore the protective effect of exogenous expansionary pressures generated by continuous positive airway pressure （CPAP） against hmg tissues of rats with chronic obstructive pulmonary disease （COPD）. Methods Forty Wistar rats were randomly divided into four groups （n ： 10） ： control group, sham group, COPD group, and COPD ＋ CPAP group. COPD rat model was developed by inhaling cigarette smoke. The pathological changes of lung tissues of different groups were observed by HE staining. The p-EGFR, p-ERK, and TGF-β1 expressions were detected by inmmnohistochemistry. The EGFR and TGF-β1 mRNA expressions were measured by RT-PCR. The p-EGFR, ERK, p-ERK, and TGF-β1 protein levels were detected by Western blotting. Results Compared with normal control group, there were significantly bronchopulmonary pathological changes in COPD group, and EGFR, ERK, and TGF-β1 expression levels and the degree of phosphorylation were also significantly enhanced （P 〈0.01）. After CPAP treatment, these indicators were significantly decreased （P 〈 0. 01 ）. The differences between the sham group and the normal control group were not statistically significant （P 〉 0.05）. Conclusion The improvement of lung inflammation of COPD rats after CPAP treatment may be relevant to the EGFR and TGF-β1 signaling pathways regulation.