Mucin1 relieves acute lung injury by inhibiting inflammation and oxidative stress

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a kind of diffuse inflammatory injury caused by various factors, characterized by respiratory distress and progressive hypoxemia. It is a common clinical critical illness. The aim of this study was to investigate the effect and mec...

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Autores principales:	Chunlin Ye, Bin Xu, Jie Yang, Yunkun Liu, Zhikai Zeng, Lingchun Xia, Quanjin Li, Guowen Zou
Formato:	article
Lenguaje:	EN
Publicado:	PAGEPress Publications 2021
Materias:	Mucin1 acute lung injury inflammation oxidative stress TLR4/NF-κB Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/418d49e2355943508be22952abb27517
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spelling	oai:doaj.org-article:418d49e2355943508be22952abb275172021-12-03T07:58:39ZMucin1 relieves acute lung injury by inhibiting inflammation and oxidative stress10.4081/ejh.2021.33311121-760X2038-8306https://doaj.org/article/418d49e2355943508be22952abb275172021-12-01T00:00:00Zhttps://www.ejh.it/index.php/ejh/article/view/3331https://doaj.org/toc/1121-760Xhttps://doaj.org/toc/2038-8306 Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a kind of diffuse inflammatory injury caused by various factors, characterized by respiratory distress and progressive hypoxemia. It is a common clinical critical illness. The aim of this study was to investigate the effect and mechanism of the Mucin1 (MUC1) gene and its recombinant protein on lipopolysaccharide (LPS)-induced ALI/ARDS. We cultured human alveolar epithelial cell line (BEAS-2B) and used MUC1 overexpression lentivirus to detect the effect of MUC1 gene on BEAS-2B cells. In addition, we used LPS to induce ALI/ARDS in C57/BL6 mice and use hematoxylin and eosin (H&E) staining to verify the effect of their modeling. Recombinant MUC1 protein was injected subcutaneously into mice. We examined the effect of MUC1 on ALI/ARDS in mice by detecting the expression of inflammatory factors and oxidative stress molecules in mouse lung tissue, bronchoalveolar lavage fluid (BALF) and serum. Overexpression of MUC1 effectively ameliorated LPS-induced damage to BEAS-2B cells. Results of H&E staining indicate that LPS successfully induced ALI/ARDS in mice and MUC1 attenuated lung injury. MUC1 also reduced the expression of inflammatory factors (IL-1β, TNF-α, IL-6 and IL-8) and oxidative stress levels in mice. In addition, LPS results in an increase in the activity of the TLR4/NF-κB signaling pathway in mice, whereas MUC1 decreased the expression of the TLR4/NF-κB signaling pathway. MUC1 inhibited the activity of TLR4/NF-κB signaling pathway and reduced the level of inflammation and oxidative stress in lung tissue of ALI mice. Chunlin YeBin XuJie YangYunkun LiuZhikai ZengLingchun XiaQuanjin LiGuowen ZouPAGEPress PublicationsarticleMucin1acute lung injuryinflammationoxidative stressTLR4/NF-κBBiology (General)QH301-705.5ENEuropean Journal of Histochemistry , Vol 65, Iss 4 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Mucin1 acute lung injury inflammation oxidative stress TLR4/NF-κB Biology (General) QH301-705.5
spellingShingle	Mucin1 acute lung injury inflammation oxidative stress TLR4/NF-κB Biology (General) QH301-705.5 Chunlin Ye Bin Xu Jie Yang Yunkun Liu Zhikai Zeng Lingchun Xia Quanjin Li Guowen Zou Mucin1 relieves acute lung injury by inhibiting inflammation and oxidative stress
description	Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a kind of diffuse inflammatory injury caused by various factors, characterized by respiratory distress and progressive hypoxemia. It is a common clinical critical illness. The aim of this study was to investigate the effect and mechanism of the Mucin1 (MUC1) gene and its recombinant protein on lipopolysaccharide (LPS)-induced ALI/ARDS. We cultured human alveolar epithelial cell line (BEAS-2B) and used MUC1 overexpression lentivirus to detect the effect of MUC1 gene on BEAS-2B cells. In addition, we used LPS to induce ALI/ARDS in C57/BL6 mice and use hematoxylin and eosin (H&E) staining to verify the effect of their modeling. Recombinant MUC1 protein was injected subcutaneously into mice. We examined the effect of MUC1 on ALI/ARDS in mice by detecting the expression of inflammatory factors and oxidative stress molecules in mouse lung tissue, bronchoalveolar lavage fluid (BALF) and serum. Overexpression of MUC1 effectively ameliorated LPS-induced damage to BEAS-2B cells. Results of H&E staining indicate that LPS successfully induced ALI/ARDS in mice and MUC1 attenuated lung injury. MUC1 also reduced the expression of inflammatory factors (IL-1β, TNF-α, IL-6 and IL-8) and oxidative stress levels in mice. In addition, LPS results in an increase in the activity of the TLR4/NF-κB signaling pathway in mice, whereas MUC1 decreased the expression of the TLR4/NF-κB signaling pathway. MUC1 inhibited the activity of TLR4/NF-κB signaling pathway and reduced the level of inflammation and oxidative stress in lung tissue of ALI mice.
format	article
author	Chunlin Ye Bin Xu Jie Yang Yunkun Liu Zhikai Zeng Lingchun Xia Quanjin Li Guowen Zou
author_facet	Chunlin Ye Bin Xu Jie Yang Yunkun Liu Zhikai Zeng Lingchun Xia Quanjin Li Guowen Zou
author_sort	Chunlin Ye
title	Mucin1 relieves acute lung injury by inhibiting inflammation and oxidative stress
title_short	Mucin1 relieves acute lung injury by inhibiting inflammation and oxidative stress
title_full	Mucin1 relieves acute lung injury by inhibiting inflammation and oxidative stress
title_fullStr	Mucin1 relieves acute lung injury by inhibiting inflammation and oxidative stress
title_full_unstemmed	Mucin1 relieves acute lung injury by inhibiting inflammation and oxidative stress
title_sort	mucin1 relieves acute lung injury by inhibiting inflammation and oxidative stress
publisher	PAGEPress Publications
publishDate	2021
url	https://doaj.org/article/418d49e2355943508be22952abb27517
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_version_	1718373383668760576

Mucin1 relieves acute lung injury by inhibiting inflammation and oxidative stress

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