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目的探讨保肺定喘汤治疗慢性阻塞性肺疾病(COPD)的可能作用机制。方法 50只大鼠随机分为正常组、模型组、中药组、西药组和中西医结合组,每组10只。除正常组外其余各组采用气道滴注脂多糖联合香烟烟雾暴露的方法制备大鼠COPD模型。造模后第29~70天中药组给予保肺定喘汤12.4 g/(kg·d)灌胃,西药组雾化吸入布地奈德混悬液50μg/(kg·d),中西医结合组同时予保肺定喘汤灌胃及雾化吸入布地奈德混悬液,正常组、模型组用4 ml(kg·d)生理盐水灌胃。干预后对各组大鼠肺小动脉进行Masson染色并检测管壁内胶原纤维及α-平滑肌肌动蛋白(α-SMA)表达变化,检测血清白细胞介素6(IL-6)含量及大鼠肺动脉磷酸化Janus激酶2(p-JAK2)和磷酸化信号转导及转录激活因子1(p-STAT1)表达情况。结果与正常组比较,模型组大鼠肺小动脉胶原纤维百分比、α-SMA阳性细胞表达显著增加,血清IL-6含量升高,肺动脉p-JAK2和p-STAT1表达显著增加(P<0.05或P<0.01)。西药组、中药组与中西医结合组肺小动脉胶原纤维百分比、α-SMA阳性细胞表达、血清IL-6含量及肺动脉p-JAK2和p-STAT1表达均较模型组显著减少(P<0.05或P<0.01);中西医结合组较中药组p-JAK2表达显著下降(P<0.05)。结论保肺定喘汤能有效减轻COPD大鼠肺血管重构,其机制可能与抑制JAK/STAT信号传导通路、调节大鼠肺动脉胶原纤维和α-SMA表达有关。
Objective To explore the possible mechanism of Baoshen Dingchuan Decoction in treating chronic obstructive pulmonary disease (COPD). Methods Fifty rats were randomly divided into normal group, model group, traditional Chinese medicine group, western medicine group and integrated traditional Chinese and western medicine group, with 10 rats in each group. Except the normal group, COPD model was established by airway instillation of lipopolysaccharide combined with cigarette smoke exposure. The rats in the TCM group were administered with 12.4 g / (kg · d) of Baofudingchuan Decoction orally on the 29th to 70th days after modeling. The western medicine group was inhaled budesonide suspension 50μg / (kg · d) At the same time, Baofudingchuan Tang was given into the stomach and inhaled budesonide suspension. In the normal group, the model group was given gavage with 4 ml (kg · d) saline. After the intervention, the pulmonary arterioles of rats in each group were subjected to Masson staining to detect the expression of collagen fibers and α-smooth muscle actin (α-SMA) in the wall of the rats. The levels of serum interleukin 6 (IL-6) Pulmonary artery phosphorylation Janus kinase 2 (p-JAK2) and phosphorylation signal transducers and activators of transcription 1 (p-STAT1) expression. Results Compared with the normal group, the percentage of collagen fibers and α-SMA positive cells in the pulmonary arterioles increased significantly in the model group and the levels of IL-6 in the pulmonary arterioles increased significantly (P <0.05 or P <0.05 or P <0.05) P <0.01). Compared with the model group, the percentages of collagen fibers, the expression of α-SMA positive cells, the level of IL-6 in serum and the expressions of p-JAK2 and p-STAT1 in pulmonary arteries of the western medicine group, the traditional Chinese medicine group and the combination of traditional Chinese and western medicine were significantly decreased (P <0.05 or P <0.01). The expression of p-JAK2 in TCM-WM group was significantly lower than that in TCM group (P <0.05). Conclusion Baofudinchuan Decoction can effectively reduce the pulmonary vascular remodeling in COPD rats. The mechanism may be related to the inhibition of JAK / STAT signaling pathway and the regulation of pulmonary artery collagen fibers and α-SMA in rats.