Fengke decoction alleviates trachea inflammation in cough variant asthma rats via SIRT1/NF-κB/NLRP3 signaling pathway
Objective To determine the effect and mechanism of Fengke decoction on trachea inflammation and lung function in rats with cough variant asthma(CVA).Methods The rat model of asthma was sensitized by 1 mL hypodermic injection of ovum protein(OVA)and aluminum hydroxide mixture,and then stimulated by atomized OVA.The rat model was treated with Fengke decoction at low dose,high dose and dexamethasone respectively and the corresponding volume of normal saline was administered by gavage in both the normal control group and the model group.The inflammatory cells in the bronchoalveolar lavage fluid(BALF)were counted by Diff-Quick method.IL-1β,IL-18,IL-17 and IL-22 cytokines in the BALF supernatant were detected by ELISA method.The changes in the lung histopathology were observed by HE staining.Western blot and q-PCR were used to detect the expression levels of SIRT1/NF-κB/NLRP3 signaling pathway in the rat lung tissues.Caspase-1 activity assay kit was used to detect Caspase-1 activity in the liver tissue.Results Compared with the normal group,the number of inflammatory cells,the content of inflammatory factors and the pathological changes shown by HE staining in the model group were obviously increased,and the protein and mRNA levels of NF-κB,NLRP3,ASC,Caspase-1,IL-1β and IL-18 were also much increased(P<0.05),while the expression level of SIRT1 was decreased.Compared with the model group,high dose Fengke decoction significantly reduced the number of inflammatory cells and the content of inflammatory factors,improved the pathological changes in the lung tissue,increased the expression level of SIRT1,and reduced the protein and mRNA levels of NF-κB,NLRP3,ASC,IL-1β and IL-18.The effect was comparable to that of dexamethasone.In addition,Fengke decoction reduced the activity of Caspase-1.Conclusion Fengke decoction can effectively alleviate trachea inflammation and improve the lung function in CVA rats via SIRT1/NF-κB/NLRP3 signaling pathway.