The Protective Effect of Naringenin on Airway Remodeling after Mycoplasma Pneumoniae Infection by Inhibiting Autophagy-Mediated Lung Inflammation and Fibrosis
Our previous study has shown that Chinese medicine, Qingfei Tongluo formula (QTF), has a significantly therapeutic effect to Mycoplasma pneumoniae (MP) pneumonia (MPP). The aim of this study was to investigate the therapeutic effect and mechanism of naringenin (NRG) on MPP which was an important com...
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Wiley
2018-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2018/8753894 |
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author | Yan Lin Dan Tan Qianna Kan Zhen Xiao Zhiyan Jiang |
author_facet | Yan Lin Dan Tan Qianna Kan Zhen Xiao Zhiyan Jiang |
author_sort | Yan Lin |
collection | DOAJ |
description | Our previous study has shown that Chinese medicine, Qingfei Tongluo formula (QTF), has a significantly therapeutic effect to Mycoplasma pneumoniae (MP) pneumonia (MPP). The aim of this study was to investigate the therapeutic effect and mechanism of naringenin (NRG) on MPP which was an important component of QTF. Here, we studied 124 children with or without MPP and compared inflammatory cytokines and fibrinogen-related protein expression with enzyme-linked immunosorbent assay. We also employed a BALB/c mouse model of MPP and divided the mice into three groups: ctrl (normal control mice), MPP (MP-infected mice), and MPP + NRG (MP-infected mice treated with NRG). BEAS-2B cells were used to confirm the relationship between autophagy, inflammation, and fibrosis. The results show proinflammatory cytokines (interleukin- [IL-] 6, IL-1β, and tumor necrosis factor-α), and transforming growth factor beta (TGF-β) expression was significantly increased after MP infection from both clinical and animal experiment. In vivo experimental confirmation showed that NRG treatment decreased MPP-induced lung injury in mice by inhibiting autophagy-mediated inflammatory cytokine expression and pulmonary fibrosis. In vitro experiments confirmed it. These results indicate that NRG treatment suppressed the inflammatory response and pulmonary fibrosis by inhibition of autophagy after MP infection. |
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institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2018-01-01 |
publisher | Wiley |
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series | Mediators of Inflammation |
spelling | doaj-art-c093fb2f2afb46288216adf597f407dd2025-02-03T06:12:15ZengWileyMediators of Inflammation0962-93511466-18612018-01-01201810.1155/2018/87538948753894The Protective Effect of Naringenin on Airway Remodeling after Mycoplasma Pneumoniae Infection by Inhibiting Autophagy-Mediated Lung Inflammation and FibrosisYan Lin0Dan Tan1Qianna Kan2Zhen Xiao3Zhiyan Jiang4Department of Pediatrics, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 725 South WanPing Road, Shanghai 200032, ChinaDepartment of Pediatrics, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 725 South WanPing Road, Shanghai 200032, ChinaDepartment of Pediatrics, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 725 South WanPing Road, Shanghai 200032, ChinaDepartment of Pediatrics, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 725 South WanPing Road, Shanghai 200032, ChinaDepartment of Pediatrics, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, 725 South WanPing Road, Shanghai 200032, ChinaOur previous study has shown that Chinese medicine, Qingfei Tongluo formula (QTF), has a significantly therapeutic effect to Mycoplasma pneumoniae (MP) pneumonia (MPP). The aim of this study was to investigate the therapeutic effect and mechanism of naringenin (NRG) on MPP which was an important component of QTF. Here, we studied 124 children with or without MPP and compared inflammatory cytokines and fibrinogen-related protein expression with enzyme-linked immunosorbent assay. We also employed a BALB/c mouse model of MPP and divided the mice into three groups: ctrl (normal control mice), MPP (MP-infected mice), and MPP + NRG (MP-infected mice treated with NRG). BEAS-2B cells were used to confirm the relationship between autophagy, inflammation, and fibrosis. The results show proinflammatory cytokines (interleukin- [IL-] 6, IL-1β, and tumor necrosis factor-α), and transforming growth factor beta (TGF-β) expression was significantly increased after MP infection from both clinical and animal experiment. In vivo experimental confirmation showed that NRG treatment decreased MPP-induced lung injury in mice by inhibiting autophagy-mediated inflammatory cytokine expression and pulmonary fibrosis. In vitro experiments confirmed it. These results indicate that NRG treatment suppressed the inflammatory response and pulmonary fibrosis by inhibition of autophagy after MP infection.http://dx.doi.org/10.1155/2018/8753894 |
spellingShingle | Yan Lin Dan Tan Qianna Kan Zhen Xiao Zhiyan Jiang The Protective Effect of Naringenin on Airway Remodeling after Mycoplasma Pneumoniae Infection by Inhibiting Autophagy-Mediated Lung Inflammation and Fibrosis Mediators of Inflammation |
title | The Protective Effect of Naringenin on Airway Remodeling after Mycoplasma Pneumoniae Infection by Inhibiting Autophagy-Mediated Lung Inflammation and Fibrosis |
title_full | The Protective Effect of Naringenin on Airway Remodeling after Mycoplasma Pneumoniae Infection by Inhibiting Autophagy-Mediated Lung Inflammation and Fibrosis |
title_fullStr | The Protective Effect of Naringenin on Airway Remodeling after Mycoplasma Pneumoniae Infection by Inhibiting Autophagy-Mediated Lung Inflammation and Fibrosis |
title_full_unstemmed | The Protective Effect of Naringenin on Airway Remodeling after Mycoplasma Pneumoniae Infection by Inhibiting Autophagy-Mediated Lung Inflammation and Fibrosis |
title_short | The Protective Effect of Naringenin on Airway Remodeling after Mycoplasma Pneumoniae Infection by Inhibiting Autophagy-Mediated Lung Inflammation and Fibrosis |
title_sort | protective effect of naringenin on airway remodeling after mycoplasma pneumoniae infection by inhibiting autophagy mediated lung inflammation and fibrosis |
url | http://dx.doi.org/10.1155/2018/8753894 |
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