Conclusion
AZM alleviated airway inflammation by inhibiting the SAPK/JNK pathway, thereby repressing AR in asthmatic mice. This study provided partial theoretical basis for clarifying asthma pathogenesis and new ideas for treating asthma.
Methods
Simulated asthmatic AR mouse model was developed by induction with ovalbumin (OVA) and intervened with AZM or dexamethasone (DEX) and anisomycin (JNK activator). Pathological changes in mouse lung tissues and AR were assessed by HE and Masson staining. The numbers of inflammatory cells, macrophages, eosinophils, neutrophils and lymphocytes in bronchoalveolar lavage fluid (BALF) were detected by Diff-Quik staining. Inflammatory factor levels (IL-6, TNF-α, IL-4) in BALF, and Collagen I, Collagen III, SAPK/JNK and p-SAPK/JNK protein levels in lung tissues were measured by ELISA and Western blot.
Objective
Asthma is a prevalent status attributing to lower respiratory tract chronic inflammation. Azithromycin (AZM) is known to be effective against asthma. Thus, this study delved into the mechanism of AZM repressing airway remodeling (AR) via the SAPK/JNK pathway in asthma.
Results
The OVA-led asthmatic mouse model was successfully established. Relative to the OVA group, AZM and DEX treatment improved pulmonary smooth muscle thickening and bronchial epithelial fibrosis, reduced inflammatory cells, macrophages, eosinophils, neutrophils and lymphocytes in BALF, inhibited inflammatory factor TNF-α, IL-6, and IL-4 levels in BALF, and down-regulated Collagen I, Collagen III, and p-SAPK/JNK protein levels in lung tissues, with no prominent difference between the two regimens. JNK activator partially reversed the protective effect of AZM against OVA-induced asthma in mice.