Study of the effect of azithromycin on airway remodeling in asthma via the SAPK/JNK pathway
Abstract 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. Methods Sim...
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2024-12-01
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Online Access: | https://doi.org/10.1186/s13019-024-03193-w |
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author | Dannv Ma Huaqing Du Yi Huang Aiwu Pan Lu Gan |
author_facet | Dannv Ma Huaqing Du Yi Huang Aiwu Pan Lu Gan |
author_sort | Dannv Ma |
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description | Abstract 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. 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. 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. 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. |
format | Article |
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institution | Kabale University |
issn | 1749-8090 |
language | English |
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series | Journal of Cardiothoracic Surgery |
spelling | doaj-art-ccac9b8e782c4d1fb52317122ce4c2692025-01-05T12:45:55ZengBMCJournal of Cardiothoracic Surgery1749-80902024-12-011911910.1186/s13019-024-03193-wStudy of the effect of azithromycin on airway remodeling in asthma via the SAPK/JNK pathwayDannv Ma0Huaqing Du1Yi Huang2Aiwu Pan3Lu Gan4Department of Internal Medicine, the Second Affiliated Hospital, Zhejiang University School of MedicineDepartment of Internal Medicine, the Second Affiliated Hospital, Zhejiang University School of MedicineDepartment of Internal Medicine, the Second Affiliated Hospital, Zhejiang University School of MedicineDepartment of Internal Medicine, the Second Affiliated Hospital, Zhejiang University School of MedicineDepartment of Internal Medicine, the Second Affiliated Hospital, Zhejiang University School of MedicineAbstract 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. 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. 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. 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.https://doi.org/10.1186/s13019-024-03193-wAzithromycinAsthmaAirway remodelingAirway inflammationStress activated protein kinases/C-jun N-terminal kinases |
spellingShingle | Dannv Ma Huaqing Du Yi Huang Aiwu Pan Lu Gan Study of the effect of azithromycin on airway remodeling in asthma via the SAPK/JNK pathway Journal of Cardiothoracic Surgery Azithromycin Asthma Airway remodeling Airway inflammation Stress activated protein kinases/C-jun N-terminal kinases |
title | Study of the effect of azithromycin on airway remodeling in asthma via the SAPK/JNK pathway |
title_full | Study of the effect of azithromycin on airway remodeling in asthma via the SAPK/JNK pathway |
title_fullStr | Study of the effect of azithromycin on airway remodeling in asthma via the SAPK/JNK pathway |
title_full_unstemmed | Study of the effect of azithromycin on airway remodeling in asthma via the SAPK/JNK pathway |
title_short | Study of the effect of azithromycin on airway remodeling in asthma via the SAPK/JNK pathway |
title_sort | study of the effect of azithromycin on airway remodeling in asthma via the sapk jnk pathway |
topic | Azithromycin Asthma Airway remodeling Airway inflammation Stress activated protein kinases/C-jun N-terminal kinases |
url | https://doi.org/10.1186/s13019-024-03193-w |
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