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Melatonin reduces IL‐33 and TSLP expression in human nasal epithelial cells by scavenging ROS directly
BACKGROUND: Chronic rhinosinusitis (CRS) is a chronic mucosal inflammation of the nasal cavity and sinuses. It is classified into CRS without nasal polyps and CRS with nasal polyps (CRSwNP). CRSwNP has high recurrence, especially CRSwNP with massive eosinophil infiltration which is mediated by type...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9933203/ https://www.ncbi.nlm.nih.gov/pubmed/36840497 http://dx.doi.org/10.1002/iid3.788 |
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author | Gong, Min‐jie Zhang, Hai‐bao Lou, Miao Wang, Yu‐sheng Ma, Rui‐ping Hu, Zhen‐zhen Zheng, Guo‐xi Zhang, Ya |
author_facet | Gong, Min‐jie Zhang, Hai‐bao Lou, Miao Wang, Yu‐sheng Ma, Rui‐ping Hu, Zhen‐zhen Zheng, Guo‐xi Zhang, Ya |
author_sort | Gong, Min‐jie |
collection | PubMed |
description | BACKGROUND: Chronic rhinosinusitis (CRS) is a chronic mucosal inflammation of the nasal cavity and sinuses. It is classified into CRS without nasal polyps and CRS with nasal polyps (CRSwNP). CRSwNP has high recurrence, especially CRSwNP with massive eosinophil infiltration which is mediated by type 2 inflammatory response. Melatonin is a hormone secreted by the pineal gland, it has powerful antioxidant and anti‐inflammatory effects in addition to regulating biological rhythms. There are no studies on melatonin for the treatment of CRS, so we aimed to explore whether melatonin could be used for the treatment of CRS. MATERIALS AND METHODS: In this study, we used melatonin to treat a cell model of CRS. Subsequently, MTT assay was performed to examine the cell viability of human nasal epithelial cells (HNEpCs), a reactive oxygen species (ROS) kit to detect ROS production, a malondialdehyde (MDA) kit to detect the MDA content in the cell culture supernatant, and an apoptosis kit and Western blot analysis to detect apoptosis. The expressions of Nrf2, HO‐1, IL‐33, TSLP, and IL‐25 were detected by Western blot analysis. RESULTS: Melatonin improved the viability of HNEpCs, reduced lipopolysaccharide‐induced ROS, reduced the MDA content, and inhibited their apoptosis. More importantly, melatonin reduced the expression of IL‐33 and TSLP, an important phenomenon for the treatment of CRSwNP. CONCLUSION: Melatonin protects HNEpCs from damage in inflammation and reduces IL‐33 and TSLP expression of HNEpCs. |
format | Online Article Text |
id | pubmed-9933203 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-99332032023-02-17 Melatonin reduces IL‐33 and TSLP expression in human nasal epithelial cells by scavenging ROS directly Gong, Min‐jie Zhang, Hai‐bao Lou, Miao Wang, Yu‐sheng Ma, Rui‐ping Hu, Zhen‐zhen Zheng, Guo‐xi Zhang, Ya Immun Inflamm Dis Short Reports BACKGROUND: Chronic rhinosinusitis (CRS) is a chronic mucosal inflammation of the nasal cavity and sinuses. It is classified into CRS without nasal polyps and CRS with nasal polyps (CRSwNP). CRSwNP has high recurrence, especially CRSwNP with massive eosinophil infiltration which is mediated by type 2 inflammatory response. Melatonin is a hormone secreted by the pineal gland, it has powerful antioxidant and anti‐inflammatory effects in addition to regulating biological rhythms. There are no studies on melatonin for the treatment of CRS, so we aimed to explore whether melatonin could be used for the treatment of CRS. MATERIALS AND METHODS: In this study, we used melatonin to treat a cell model of CRS. Subsequently, MTT assay was performed to examine the cell viability of human nasal epithelial cells (HNEpCs), a reactive oxygen species (ROS) kit to detect ROS production, a malondialdehyde (MDA) kit to detect the MDA content in the cell culture supernatant, and an apoptosis kit and Western blot analysis to detect apoptosis. The expressions of Nrf2, HO‐1, IL‐33, TSLP, and IL‐25 were detected by Western blot analysis. RESULTS: Melatonin improved the viability of HNEpCs, reduced lipopolysaccharide‐induced ROS, reduced the MDA content, and inhibited their apoptosis. More importantly, melatonin reduced the expression of IL‐33 and TSLP, an important phenomenon for the treatment of CRSwNP. CONCLUSION: Melatonin protects HNEpCs from damage in inflammation and reduces IL‐33 and TSLP expression of HNEpCs. John Wiley and Sons Inc. 2023-02-16 /pmc/articles/PMC9933203/ /pubmed/36840497 http://dx.doi.org/10.1002/iid3.788 Text en © 2023 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Short Reports Gong, Min‐jie Zhang, Hai‐bao Lou, Miao Wang, Yu‐sheng Ma, Rui‐ping Hu, Zhen‐zhen Zheng, Guo‐xi Zhang, Ya Melatonin reduces IL‐33 and TSLP expression in human nasal epithelial cells by scavenging ROS directly |
title | Melatonin reduces IL‐33 and TSLP expression in human nasal epithelial cells by scavenging ROS directly |
title_full | Melatonin reduces IL‐33 and TSLP expression in human nasal epithelial cells by scavenging ROS directly |
title_fullStr | Melatonin reduces IL‐33 and TSLP expression in human nasal epithelial cells by scavenging ROS directly |
title_full_unstemmed | Melatonin reduces IL‐33 and TSLP expression in human nasal epithelial cells by scavenging ROS directly |
title_short | Melatonin reduces IL‐33 and TSLP expression in human nasal epithelial cells by scavenging ROS directly |
title_sort | melatonin reduces il‐33 and tslp expression in human nasal epithelial cells by scavenging ros directly |
topic | Short Reports |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9933203/ https://www.ncbi.nlm.nih.gov/pubmed/36840497 http://dx.doi.org/10.1002/iid3.788 |
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