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Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway

Chronic obstructive pulmonary disease (COPD) is a prevalent and long-term airway disease. It has been reported that fucoxanthin (FX) exhibits anti-inflammatory and antioxidant effects. However, the underlying mechanism of FX in COPD remains unknown. Therefore, to investigate the effect of FX on COPD...

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Autores principales: Chen, Shaolei, Zhu, Lin, Li, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9798150/
https://www.ncbi.nlm.nih.gov/pubmed/36605523
http://dx.doi.org/10.3892/etm.2022.11768
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author Chen, Shaolei
Zhu, Lin
Li, Jun
author_facet Chen, Shaolei
Zhu, Lin
Li, Jun
author_sort Chen, Shaolei
collection PubMed
description Chronic obstructive pulmonary disease (COPD) is a prevalent and long-term airway disease. It has been reported that fucoxanthin (FX) exhibits anti-inflammatory and antioxidant effects. However, the underlying mechanism of FX in COPD remains unknown. Therefore, to investigate the effect of FX on COPD, BEAS-2B cells were treated with cigarette smoke extract (CSE). The viability of BEAS-2B cells treated with increasing doses of FX was assessed by Cell Counting Kit-8. Lactate dehydrogenase (LDH) levels were measured using a corresponding kit. In addition, ELISA was carried out to detect the content of TNF-α, IL-1β and IL-6. Additionally, a TUNEL assay and western blot analysis were performed to assess the cell apoptosis rate. Furthermore, 2',7'-dichlorodihydrofluorescein diacetate was used to measure reactive oxygen species levels, while the contents of oxidative stress-associated indexes were determined using the corresponding kits. Bioinformatics analysis using the search tool for interactions of chemicals database predicted that peroxisome proliferator-activated receptor γ (PPARγ) may be a target of FX. The binding capacity of FTX with PPARγ was confirmed by molecular docking. The protein expression levels of the PPARγ/NF-κB signaling-associated factors were detected by western blot analysis. Finally, the regulatory mechanism of FX in COPD was revealed following cell treatment with the PPARγ inhibitor, T0070907. The results demonstrated that FX enhanced CSE-induced BEAS-2B cell viability and attenuated CSE-induced BEAS-2B cell inflammation and oxidative damage, possibly via triggering PPARγ/NF-κB signaling. Pre-treatment of BEAS-2B cells with the PPARγ inhibitor, T0070907, could reverse the protective effects of FX on CSE-induced BEAS-2B cells. Overall, the present study suggested that FX could ameliorate oxidative damage as well as inflammation in CSE-treated human bronchial epithelial in patients with COPD via modulating the PPARγ/NF-κB signaling pathway.
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spelling pubmed-97981502023-01-04 Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway Chen, Shaolei Zhu, Lin Li, Jun Exp Ther Med Articles Chronic obstructive pulmonary disease (COPD) is a prevalent and long-term airway disease. It has been reported that fucoxanthin (FX) exhibits anti-inflammatory and antioxidant effects. However, the underlying mechanism of FX in COPD remains unknown. Therefore, to investigate the effect of FX on COPD, BEAS-2B cells were treated with cigarette smoke extract (CSE). The viability of BEAS-2B cells treated with increasing doses of FX was assessed by Cell Counting Kit-8. Lactate dehydrogenase (LDH) levels were measured using a corresponding kit. In addition, ELISA was carried out to detect the content of TNF-α, IL-1β and IL-6. Additionally, a TUNEL assay and western blot analysis were performed to assess the cell apoptosis rate. Furthermore, 2',7'-dichlorodihydrofluorescein diacetate was used to measure reactive oxygen species levels, while the contents of oxidative stress-associated indexes were determined using the corresponding kits. Bioinformatics analysis using the search tool for interactions of chemicals database predicted that peroxisome proliferator-activated receptor γ (PPARγ) may be a target of FX. The binding capacity of FTX with PPARγ was confirmed by molecular docking. The protein expression levels of the PPARγ/NF-κB signaling-associated factors were detected by western blot analysis. Finally, the regulatory mechanism of FX in COPD was revealed following cell treatment with the PPARγ inhibitor, T0070907. The results demonstrated that FX enhanced CSE-induced BEAS-2B cell viability and attenuated CSE-induced BEAS-2B cell inflammation and oxidative damage, possibly via triggering PPARγ/NF-κB signaling. Pre-treatment of BEAS-2B cells with the PPARγ inhibitor, T0070907, could reverse the protective effects of FX on CSE-induced BEAS-2B cells. Overall, the present study suggested that FX could ameliorate oxidative damage as well as inflammation in CSE-treated human bronchial epithelial in patients with COPD via modulating the PPARγ/NF-κB signaling pathway. D.A. Spandidos 2022-12-14 /pmc/articles/PMC9798150/ /pubmed/36605523 http://dx.doi.org/10.3892/etm.2022.11768 Text en Copyright: © Chen et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Chen, Shaolei
Zhu, Lin
Li, Jun
Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway
title Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway
title_full Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway
title_fullStr Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway
title_full_unstemmed Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway
title_short Fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the PPARγ/NF‑κB signaling pathway
title_sort fucoxanthin ameliorates oxidative injury and inflammation of human bronchial epithelial cells induced by cigarette smoke extract via the pparγ/nf‑κb signaling pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9798150/
https://www.ncbi.nlm.nih.gov/pubmed/36605523
http://dx.doi.org/10.3892/etm.2022.11768
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