Zhuye Shigao Decoction Combined with Qingqi Huatan Pills in Alleviating the Acute Exacerbation of Chronic Obstructive Pulmonary Disease (Phlegm-Heat Stagnating in the Lungs) via the IL-6-Mediated JAK1/STAT3 Signaling Pathway

Chronic obstructive pulmonary disease (COPD) is a chronic disease with a long course which is often induced by an acute exacerbation of the disease by a respiratory tract infection. We aimed to explore the effect of Zhuye Shigao Decoction combined with Qingqi Huatan Pills on the regulation of the interleukin (IL)-6-mediated JAK1/STAT3 signaling pathway in rats with an acute exacerbation of COPD (phlegm-heat stagnating in the lungs). A model of COPD rats with lung phlegm-heat stagnation was established by smoking and intratracheal injection of lipopolysaccharide (LPS). The rats were randomly divided into eight groups: normal control, model control, three doses of herbs group, and three doses of herbs + itacitinib groups. The lung function indexes were measured by using a lung function tester, and changes in pathological features of all groups were observed by hematoxylin-eosin (HE) staining. The mRNA expression and protein expression levels in lung tissues were determined by real-time quantitative polymerase chain reaction (RT-qPCR), western blot, and immunohistochemical assay, respectively. Following treatment, IL-6 expression in lung tissues was significantly reduced compared with the model group. The results demonstrated that the medication was effective in alleviating the persistent airflow limitation and pathological features in COPD rats. Expression of JAK1/STAT3 in lung tissues was remarkably decreased. The JAK1/STAT3 pathway was inhibited, while SOCS3 expression was upregulated in the drug-treated groups compared with model control. However, after the addition of itacitinib (JAK1 inhibitor), the efficacy in each group was evidently impaired compared with herbs alone. Taken together, Zhuye Shigao Decoction combined with Qingqi Huatan Pills could improve the persistent airflow limitation and reduce lung inflammation and pathological changes of COPD possibly by regulating the expression of the IL-6-mediated JAK1/STAT3 pathway.