STAT3 and Nrf2 pathways modulate the protective effect of verapamil on lung injury of diabetic rats

Objective. We aimed to assess the protective role of verapamil, L-type calcium channel blockers, against early lung damage in diabetic rats. Lung injury has recently been recognized as a consequent complication of diabetes mellitus. Hyperglycemia induces inflammatory changes in lung tissue early in...

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Autores principales:	Mohamed Mervat Z., Hafez Heba M., Mohamed Hanaa H., Zenhom Nagwa M.
Formato:	article
Lenguaje:	EN
Publicado:	Sciendo 2018
Materias:	streptozotocin verapamil lung stat3 tnfα nrf2 Diseases of the endocrine glands. Clinical endocrinology RC648-665
Acceso en línea:	https://doaj.org/article/611503427def421bb9516e65843b2aba
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spelling	oai:doaj.org-article:611503427def421bb9516e65843b2aba2021-12-02T19:07:36ZSTAT3 and Nrf2 pathways modulate the protective effect of verapamil on lung injury of diabetic rats1336-032910.2478/enr-2018-0024https://doaj.org/article/611503427def421bb9516e65843b2aba2018-10-01T00:00:00Zhttps://doi.org/10.2478/enr-2018-0024https://doaj.org/toc/1336-0329Objective. We aimed to assess the protective role of verapamil, L-type calcium channel blockers, against early lung damage in diabetic rats. Lung injury has recently been recognized as a consequent complication of diabetes mellitus. Hyperglycemia induces inflammatory changes in lung tissue early in the disease. Methods. Twenty four adult male rats were grouped into control, diabetic, diabetic treated with verapamil, and verapamil control. Streptozotocin (STZ) was used to induce diabetes. Oxidative parameters and antioxidative mechanisms were assessed in lung homogenate. Tumor necrosis factor alpha (TNFα) protein was measured as a pro-inflammatory mediator. Signal transducer and activator of transcription 3 (STAT3) gene expression and nuclear erythroid factor 2 (Nrf2) immunoexpression were screened. Results. The lung showed oxidative damage and inflammatory infiltration in STZ diabetic rats early at 2 weeks. The parameters significantly improved in lung tissue treated with verapamil. Histopathology of the lung tissue confirmed the results. Inhibition of STAT3/TNFα pathway was involved in the protection offered by verapamil. Activation of Nrf2 together with an increasing antioxidant capacity of diabetic lung significantly ameliorates the injury induced by diabetes. Conclusions. Verapamil afforded protection in diabetic lung injury. The protection was mediated by the anti-inflammatory and antioxidant effects of verapamil.Mohamed Mervat Z.Hafez Heba M.Mohamed Hanaa H.Zenhom Nagwa M.Sciendoarticlestreptozotocinverapamillungstat3tnfαnrf2Diseases of the endocrine glands. Clinical endocrinologyRC648-665ENEndocrine Regulations, Vol 52, Iss 4, Pp 192-198 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	streptozotocin verapamil lung stat3 tnfα nrf2 Diseases of the endocrine glands. Clinical endocrinology RC648-665
spellingShingle	streptozotocin verapamil lung stat3 tnfα nrf2 Diseases of the endocrine glands. Clinical endocrinology RC648-665 Mohamed Mervat Z. Hafez Heba M. Mohamed Hanaa H. Zenhom Nagwa M. STAT3 and Nrf2 pathways modulate the protective effect of verapamil on lung injury of diabetic rats
description	Objective. We aimed to assess the protective role of verapamil, L-type calcium channel blockers, against early lung damage in diabetic rats. Lung injury has recently been recognized as a consequent complication of diabetes mellitus. Hyperglycemia induces inflammatory changes in lung tissue early in the disease. Methods. Twenty four adult male rats were grouped into control, diabetic, diabetic treated with verapamil, and verapamil control. Streptozotocin (STZ) was used to induce diabetes. Oxidative parameters and antioxidative mechanisms were assessed in lung homogenate. Tumor necrosis factor alpha (TNFα) protein was measured as a pro-inflammatory mediator. Signal transducer and activator of transcription 3 (STAT3) gene expression and nuclear erythroid factor 2 (Nrf2) immunoexpression were screened. Results. The lung showed oxidative damage and inflammatory infiltration in STZ diabetic rats early at 2 weeks. The parameters significantly improved in lung tissue treated with verapamil. Histopathology of the lung tissue confirmed the results. Inhibition of STAT3/TNFα pathway was involved in the protection offered by verapamil. Activation of Nrf2 together with an increasing antioxidant capacity of diabetic lung significantly ameliorates the injury induced by diabetes. Conclusions. Verapamil afforded protection in diabetic lung injury. The protection was mediated by the anti-inflammatory and antioxidant effects of verapamil.
format	article
author	Mohamed Mervat Z. Hafez Heba M. Mohamed Hanaa H. Zenhom Nagwa M.
author_facet	Mohamed Mervat Z. Hafez Heba M. Mohamed Hanaa H. Zenhom Nagwa M.
author_sort	Mohamed Mervat Z.
title	STAT3 and Nrf2 pathways modulate the protective effect of verapamil on lung injury of diabetic rats
title_short	STAT3 and Nrf2 pathways modulate the protective effect of verapamil on lung injury of diabetic rats
title_full	STAT3 and Nrf2 pathways modulate the protective effect of verapamil on lung injury of diabetic rats
title_fullStr	STAT3 and Nrf2 pathways modulate the protective effect of verapamil on lung injury of diabetic rats
title_full_unstemmed	STAT3 and Nrf2 pathways modulate the protective effect of verapamil on lung injury of diabetic rats
title_sort	stat3 and nrf2 pathways modulate the protective effect of verapamil on lung injury of diabetic rats
publisher	Sciendo
publishDate	2018
url	https://doaj.org/article/611503427def421bb9516e65843b2aba
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STAT3 and Nrf2 pathways modulate the protective effect of verapamil on lung injury of diabetic rats

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