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[目的]探讨健脾益肺化痰方对慢性阻塞性肺疾病(COPD)气道黏液高分泌的改善机制。[方法]采用烟熏法建立COPD大鼠模型,随机分为正常组、模型组、健脾益肺方组、化痰方组、健脾益肺化痰方组及羧甲司坦组。正常组、模型组灌胃生理盐水,各给药组灌胃相应药物,连续28 d。酶联免疫吸附(ELISA)法检测肺泡灌洗液肿瘤坏死因子-α(TNF-α)含量,蛋白质印迹(Western Blot)法检测肺组织表皮生长因子受体(EGFR)、磷脂酰肌醇-3激酶(PI3K)和丝氨酸苏氨酸激酶(AKT)磷酸化水平。[结果]与正常组比较,模型组大鼠TNF-α含量升高,EGFR、PI3K和AKT磷酸化增强(P<0.01);与模型组比较,各给药组TNF-α含量显著下降(P<0.01或P<0.05),EGFR、PI3K和AKT磷酸化显著下降(P<0.01)或有下降趋势。[结论]健脾益肺化痰方改善COPD大鼠气道黏液高分泌,与抑制TNF-α等信号分子有关,且“标本兼治”的作用优于单一“治本”、“治标”。
[Objective] To investigate the mechanism of improving the airway mucus hypersecretion in chronic obstructive pulmonary disease (COPD) by using “Jianpi Yifei Huatan Fang”. [Method] COPD rat model was established by smoking method and randomly divided into normal group, model group, Jianpi Yifei Fang group, Huatan Fang group, Jianpi Yifei Huatan Fang group and carbocisteine group. In the normal group, the model group was given normal saline by intragastric administration, and the corresponding drug was given to each model group for 28 consecutive days. The levels of tumor necrosis factor-α (TNF-α) in the bronchoalveolar lavage fluid were detected by enzyme linked immunosorbent assay (ELISA). The expressions of epidermal growth factor receptor (EGFR), phosphatidylinositol 3 (PI3K) and serine threonine kinase (AKT) phosphorylation levels. [Results] Compared with the normal group, the content of TNF-α and the phosphorylation of EGFR, PI3K and AKT in the model group were significantly increased (P <0.01). Compared with the model group, the content of TNF- <0.01 or P <0.05). The phosphorylation of EGFR, PI3K and AKT decreased significantly (P <0.01) or decreased. [Conclusion] Jianpi Yifei Huatan Fang can ameliorate the airway mucus hypersecretion in COPD rats, which is related to the inhibition of TNF-α and other signaling molecules, and its effect is better than that of single “ Palliative ”.