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Interleukin-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species-dependent lipid peroxidation and disrupting iron homeostasis

Asthma occurs accompanied by the ferroptosis in bronchial epithelial cells, during which Interleukin-6 (IL-6) plays a key role. However, the associations between IL-6, ferroptosis and asthma have not been reported. Bronchial epithelial cells BEAS-2B cells were induced by different concentrations of...

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Autores principales: Han, Fei, Li, Shijie, Yang, Yankun, Bai, Zhonghu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806540/
https://www.ncbi.nlm.nih.gov/pubmed/34402724
http://dx.doi.org/10.1080/21655979.2021.1964158
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author Han, Fei
Li, Shijie
Yang, Yankun
Bai, Zhonghu
author_facet Han, Fei
Li, Shijie
Yang, Yankun
Bai, Zhonghu
author_sort Han, Fei
collection PubMed
description Asthma occurs accompanied by the ferroptosis in bronchial epithelial cells, during which Interleukin-6 (IL-6) plays a key role. However, the associations between IL-6, ferroptosis and asthma have not been reported. Bronchial epithelial cells BEAS-2B cells were induced by different concentrations of IL-6 and cell viability was detected by MTT assay. The TBARS production rate was detected by corresponding kit. The expression of oxidative stress-related indexes was detected by ELISA. The Iron Assay Kits detected total iron levels and ferrous ion (Fe(2+)) levels. Labile iron pool assay was used to detect the cell unstable iron pool. The expression of ferroptosis-related proteins was detected by Western blot. To further examine the mechanism of action, ferroptosis inhibitor Ferrostatin 1 (Fer-1), antioxidant NAC, and the iron supplement Fe were added. We found that IL-6 decreased the activity, promoted lipid peroxidation, disrupted iron homeostasis of BEAS-2B cells, and induced iron death in bronchial epithelial BEAS-2B cells. However, pretreatment with Ferrostatin-1 (Fer-1) and antioxidant NAC partially reversed the effect of IL-6 on lipid peroxidation and ferroptosis in BEAS-2B cells, while Fe augmented the effect. Overall, IL-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species (ROS)-dependent lipid peroxidation and disrupting iron homeostasis.
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spelling pubmed-88065402022-02-02 Interleukin-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species-dependent lipid peroxidation and disrupting iron homeostasis Han, Fei Li, Shijie Yang, Yankun Bai, Zhonghu Bioengineered Research Paper Asthma occurs accompanied by the ferroptosis in bronchial epithelial cells, during which Interleukin-6 (IL-6) plays a key role. However, the associations between IL-6, ferroptosis and asthma have not been reported. Bronchial epithelial cells BEAS-2B cells were induced by different concentrations of IL-6 and cell viability was detected by MTT assay. The TBARS production rate was detected by corresponding kit. The expression of oxidative stress-related indexes was detected by ELISA. The Iron Assay Kits detected total iron levels and ferrous ion (Fe(2+)) levels. Labile iron pool assay was used to detect the cell unstable iron pool. The expression of ferroptosis-related proteins was detected by Western blot. To further examine the mechanism of action, ferroptosis inhibitor Ferrostatin 1 (Fer-1), antioxidant NAC, and the iron supplement Fe were added. We found that IL-6 decreased the activity, promoted lipid peroxidation, disrupted iron homeostasis of BEAS-2B cells, and induced iron death in bronchial epithelial BEAS-2B cells. However, pretreatment with Ferrostatin-1 (Fer-1) and antioxidant NAC partially reversed the effect of IL-6 on lipid peroxidation and ferroptosis in BEAS-2B cells, while Fe augmented the effect. Overall, IL-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species (ROS)-dependent lipid peroxidation and disrupting iron homeostasis. Taylor & Francis 2021-08-17 /pmc/articles/PMC8806540/ /pubmed/34402724 http://dx.doi.org/10.1080/21655979.2021.1964158 Text en © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Han, Fei
Li, Shijie
Yang, Yankun
Bai, Zhonghu
Interleukin-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species-dependent lipid peroxidation and disrupting iron homeostasis
title Interleukin-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species-dependent lipid peroxidation and disrupting iron homeostasis
title_full Interleukin-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species-dependent lipid peroxidation and disrupting iron homeostasis
title_fullStr Interleukin-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species-dependent lipid peroxidation and disrupting iron homeostasis
title_full_unstemmed Interleukin-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species-dependent lipid peroxidation and disrupting iron homeostasis
title_short Interleukin-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species-dependent lipid peroxidation and disrupting iron homeostasis
title_sort interleukin-6 promotes ferroptosis in bronchial epithelial cells by inducing reactive oxygen species-dependent lipid peroxidation and disrupting iron homeostasis
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806540/
https://www.ncbi.nlm.nih.gov/pubmed/34402724
http://dx.doi.org/10.1080/21655979.2021.1964158
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