十味咳喘方改善慢性阻塞性肺疾病气道黏液高分泌的作用机制OACHSSCD

Objective:To evaluate the expectorant,antitussive,and anti-inflammatory effects of Shiwei Kechuan Formula and ex-plore its mechanisms of action in improving airway mucus hypersecretion in chronic obstructive pulmonary disease(COPD).Meth-ods:Mice were administered Shiwei Kechuan Formula by gavage at crude drug doses of 8.5,17,and 34 g/kg.The expectorant,anti-tussive,and anti-inflammatory effects were evaluated using the phenol red airway excretion test,concentrated ammonium hydroxide-induced cough test,and xylene-induced ear swelling test,respectively.A COPD model was established by cigarette smoke exposure combined with airway instillation of lipopolysaccharide(LPS).The levels of mucins(MUC)5AC and MUC5B in bronchoalveolar lavage fluid(BALF)were measured by enzyme-linked immunosorbent assay(ELISA).The mRNA expression levels of MUC5AC and MUC5B in lung tissue were determined by quantitative reverse transcription polymerase chain reaction(RT-qPCR).The ex-pression levels of inhibitor of κB kinase β(IKKβ),nuclear factor-KB(NF-κB)p65,phosphorylated inhibitor of κBα(p-IκBα),and inhibitor of κBα(IκBα)in lung tissue were analyzed by Western blot(WB).Pathological changes in lung tissue were observed by hematoxylin-eosin(HE)staining.Results:Shiwei Kechuan Formula significantly increased phenol red airway excretion,prolonged the latency period of concentrated ammonium hydroxide-induced cough,reduced the number of coughs,and decreased the degree of xylene-induced ear swelling(P＜0.05).The formula significantly improved pathological changes in the lung tissue of COPD model mice,reduced MUC5AC and MUC5B levels in BALF,downregulated MUC5AC and MUC5B mRNA expression in lung tissue,inhib-ited IKKβ expression,reduced NF-κB p65 expression,decreased the phosphorylation level of Iκ Bα,anid inhibited its degradation(P＜0.05).Conclusion:Shiwei Kechuan Formula has significant expectorant,antitussive,and anti-inflammatory effects and can improve airway mucus hypersecretion in COPD model mice.This mechanism may be associated with inhibition of NF-κB signaling pathway activation.