Telmisartan mitigates lipopolysaccharide (LPS)-induced production of mucin 5AC (MUC5AC) through increasing suppressor of cytokine signaling 1 (SOCS1)

Acute lung injury (ALI) is a serious clinical pulmonary disease. The pathogenesis of ALI is related to the excessive release of inflammatory factors and upregulation of mucin 5AC (MUC5AC). Telmisartan is a novel antihypertension agent that exerts promising anti-inflammatory effects. The purpose of t...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Ling Chen, Jiajia Xu, Meiyu Deng, Yanling Liang, Jinfu Ma, Linghui Zhang, Yijie Wang, Jinping Zhang
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	acute lung injury telmisartan inflammation mucin 5ac (muc5ac) suppressors of cytokine signaling 1 (socs1) Biotechnology TP248.13-248.65
Acceso en línea:	https://doaj.org/article/e77a2296a10f469487182329fbab81c5
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:e77a2296a10f469487182329fbab81c5
record_format	dspace
spelling	oai:doaj.org-article:e77a2296a10f469487182329fbab81c52021-11-04T15:51:53ZTelmisartan mitigates lipopolysaccharide (LPS)-induced production of mucin 5AC (MUC5AC) through increasing suppressor of cytokine signaling 1 (SOCS1)2165-59792165-598710.1080/21655979.2021.1943605https://doaj.org/article/e77a2296a10f469487182329fbab81c52021-01-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1943605https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Acute lung injury (ALI) is a serious clinical pulmonary disease. The pathogenesis of ALI is related to the excessive release of inflammatory factors and upregulation of mucin 5AC (MUC5AC). Telmisartan is a novel antihypertension agent that exerts promising anti-inflammatory effects. The purpose of this study is to investigate whether Telmisartan has a protective role in lipopolysaccharide (LPS)-induced MUC5AC expression and to explore the underlying mechanism in human bronchial epithelial cells. Firstly, the decreased cell viability, elevated release of lactate dehydrogenase (LDH), and excessively released inflammatory factors tumor necrosis factor-α (TNF-α), interleukin- 6 (IL-6), and transforming growth factor-β (TGF)-β in bronchial BEAS-2B epithelial cells induced by stimulation with LPS were significantly reversed by the introduction of Telmisartan. Secondly, the upregulated MUC5AC and downregulated suppressor of cytokine signaling 1 (SOCS1) caused by stimulation with LPS were dramatically reversed by Telmisartan. Notably, treatment with Telmisartan attenuated LPS-induced activation of nuclear factor κ-B (NF-κB). Lastly, silencing of SOCS1 abolished the protective effects of Telmisartan against LPS-induced production of MUC5AC and the activation of NF-κB. Based on these findings, we conclude that Telmisartan displayed a protective effect against LPS by improving mitochondrial function, mitigating inflammatory response, and reducing the production of mucin 5AC by regulating the SOCS1/NF-κB axis in human bronchial epithelial cells.Ling ChenJiajia XuMeiyu DengYanling LiangJinfu MaLinghui ZhangYijie WangJinping ZhangTaylor & Francis Grouparticleacute lung injurytelmisartaninflammationmucin 5ac (muc5ac)suppressors of cytokine signaling 1 (socs1)BiotechnologyTP248.13-248.65ENBioengineered, Vol 12, Iss 1, Pp 3912-3923 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	acute lung injury telmisartan inflammation mucin 5ac (muc5ac) suppressors of cytokine signaling 1 (socs1) Biotechnology TP248.13-248.65
spellingShingle	acute lung injury telmisartan inflammation mucin 5ac (muc5ac) suppressors of cytokine signaling 1 (socs1) Biotechnology TP248.13-248.65 Ling Chen Jiajia Xu Meiyu Deng Yanling Liang Jinfu Ma Linghui Zhang Yijie Wang Jinping Zhang Telmisartan mitigates lipopolysaccharide (LPS)-induced production of mucin 5AC (MUC5AC) through increasing suppressor of cytokine signaling 1 (SOCS1)
description	Acute lung injury (ALI) is a serious clinical pulmonary disease. The pathogenesis of ALI is related to the excessive release of inflammatory factors and upregulation of mucin 5AC (MUC5AC). Telmisartan is a novel antihypertension agent that exerts promising anti-inflammatory effects. The purpose of this study is to investigate whether Telmisartan has a protective role in lipopolysaccharide (LPS)-induced MUC5AC expression and to explore the underlying mechanism in human bronchial epithelial cells. Firstly, the decreased cell viability, elevated release of lactate dehydrogenase (LDH), and excessively released inflammatory factors tumor necrosis factor-α (TNF-α), interleukin- 6 (IL-6), and transforming growth factor-β (TGF)-β in bronchial BEAS-2B epithelial cells induced by stimulation with LPS were significantly reversed by the introduction of Telmisartan. Secondly, the upregulated MUC5AC and downregulated suppressor of cytokine signaling 1 (SOCS1) caused by stimulation with LPS were dramatically reversed by Telmisartan. Notably, treatment with Telmisartan attenuated LPS-induced activation of nuclear factor κ-B (NF-κB). Lastly, silencing of SOCS1 abolished the protective effects of Telmisartan against LPS-induced production of MUC5AC and the activation of NF-κB. Based on these findings, we conclude that Telmisartan displayed a protective effect against LPS by improving mitochondrial function, mitigating inflammatory response, and reducing the production of mucin 5AC by regulating the SOCS1/NF-κB axis in human bronchial epithelial cells.
format	article
author	Ling Chen Jiajia Xu Meiyu Deng Yanling Liang Jinfu Ma Linghui Zhang Yijie Wang Jinping Zhang
author_facet	Ling Chen Jiajia Xu Meiyu Deng Yanling Liang Jinfu Ma Linghui Zhang Yijie Wang Jinping Zhang
author_sort	Ling Chen
title	Telmisartan mitigates lipopolysaccharide (LPS)-induced production of mucin 5AC (MUC5AC) through increasing suppressor of cytokine signaling 1 (SOCS1)
title_short	Telmisartan mitigates lipopolysaccharide (LPS)-induced production of mucin 5AC (MUC5AC) through increasing suppressor of cytokine signaling 1 (SOCS1)
title_full	Telmisartan mitigates lipopolysaccharide (LPS)-induced production of mucin 5AC (MUC5AC) through increasing suppressor of cytokine signaling 1 (SOCS1)
title_fullStr	Telmisartan mitigates lipopolysaccharide (LPS)-induced production of mucin 5AC (MUC5AC) through increasing suppressor of cytokine signaling 1 (SOCS1)
title_full_unstemmed	Telmisartan mitigates lipopolysaccharide (LPS)-induced production of mucin 5AC (MUC5AC) through increasing suppressor of cytokine signaling 1 (SOCS1)
title_sort	telmisartan mitigates lipopolysaccharide (lps)-induced production of mucin 5ac (muc5ac) through increasing suppressor of cytokine signaling 1 (socs1)
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/e77a2296a10f469487182329fbab81c5
work_keys_str_mv	AT lingchen telmisartanmitigateslipopolysaccharidelpsinducedproductionofmucin5acmuc5acthroughincreasingsuppressorofcytokinesignaling1socs1 AT jiajiaxu telmisartanmitigateslipopolysaccharidelpsinducedproductionofmucin5acmuc5acthroughincreasingsuppressorofcytokinesignaling1socs1 AT meiyudeng telmisartanmitigateslipopolysaccharidelpsinducedproductionofmucin5acmuc5acthroughincreasingsuppressorofcytokinesignaling1socs1 AT yanlingliang telmisartanmitigateslipopolysaccharidelpsinducedproductionofmucin5acmuc5acthroughincreasingsuppressorofcytokinesignaling1socs1 AT jinfuma telmisartanmitigateslipopolysaccharidelpsinducedproductionofmucin5acmuc5acthroughincreasingsuppressorofcytokinesignaling1socs1 AT linghuizhang telmisartanmitigateslipopolysaccharidelpsinducedproductionofmucin5acmuc5acthroughincreasingsuppressorofcytokinesignaling1socs1 AT yijiewang telmisartanmitigateslipopolysaccharidelpsinducedproductionofmucin5acmuc5acthroughincreasingsuppressorofcytokinesignaling1socs1 AT jinpingzhang telmisartanmitigateslipopolysaccharidelpsinducedproductionofmucin5acmuc5acthroughincreasingsuppressorofcytokinesignaling1socs1
_version_	1718444747224252416

Telmisartan mitigates lipopolysaccharide (LPS)-induced production of mucin 5AC (MUC5AC) through increasing suppressor of cytokine signaling 1 (SOCS1)

Ejemplares similares