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The protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunction

Excessive oxidative stress, inflammation, and myocardial hypertrophy have been associated with diabetic cardiomyopathy (DCM). S14G-humanin (HNG) is a potent humanin analogue that has demonstrated cytoprotective effects in a variety of cells and tissues. However, the pharmacological function of HNG i...

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Autores principales: Chen, Xiaopan, Yun, Chuan, Zheng, Hailong, Chen, Xu, Han, Qianfei, Pan, Hua, Wang, Yang, Zhong, Jianghua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806847/
https://www.ncbi.nlm.nih.gov/pubmed/34506248
http://dx.doi.org/10.1080/21655979.2021.1964894
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author Chen, Xiaopan
Yun, Chuan
Zheng, Hailong
Chen, Xu
Han, Qianfei
Pan, Hua
Wang, Yang
Zhong, Jianghua
author_facet Chen, Xiaopan
Yun, Chuan
Zheng, Hailong
Chen, Xu
Han, Qianfei
Pan, Hua
Wang, Yang
Zhong, Jianghua
author_sort Chen, Xiaopan
collection PubMed
description Excessive oxidative stress, inflammation, and myocardial hypertrophy have been associated with diabetic cardiomyopathy (DCM). S14G-humanin (HNG) is a potent humanin analogue that has demonstrated cytoprotective effects in a variety of cells and tissues. However, the pharmacological function of HNG in diabetic cardiomyopathy has not yet been reported. In the present study, we investigated the protective effects of HNG against streptozotocin (STZ)-induced cardiac dysfunction in diabetic mice. Myocardial hypertrophy in diabetic mice was determined using Wheat Gem Agglutinin (WGA) staining. The heart function was measured with Echocardiographic imaging. Levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) proteins in plasma were measured using enzyme-linked immunosorbent assay (ELISA) kits. Protein expression of Phosphorylated p38/p38 was determined using western blots. We found that HNG treatment attenuated the STZ-induced myocardial hypertrophy and significantly improved heart function. Also, its treatment proved effective as it reduced the levels of several myocardial injury indicators, including creatine kinase-MB (CK-MB), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and both the cardiac and plasma levels of TNF-α and IL-6, highlighting its effect on the STZ-induced myocardial injury. Lastly, HNG suppressed the activation of the p38/nuclear factor kappa-B (NF-κB) signaling pathway. S14G humanin possesses protective effects against streptozotocin-induced cardiac dysfunction through inhibiting the activation of the p38/NF-κB signaling pathway.
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spelling pubmed-88068472022-02-02 The protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunction Chen, Xiaopan Yun, Chuan Zheng, Hailong Chen, Xu Han, Qianfei Pan, Hua Wang, Yang Zhong, Jianghua Bioengineered Research Paper Excessive oxidative stress, inflammation, and myocardial hypertrophy have been associated with diabetic cardiomyopathy (DCM). S14G-humanin (HNG) is a potent humanin analogue that has demonstrated cytoprotective effects in a variety of cells and tissues. However, the pharmacological function of HNG in diabetic cardiomyopathy has not yet been reported. In the present study, we investigated the protective effects of HNG against streptozotocin (STZ)-induced cardiac dysfunction in diabetic mice. Myocardial hypertrophy in diabetic mice was determined using Wheat Gem Agglutinin (WGA) staining. The heart function was measured with Echocardiographic imaging. Levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) proteins in plasma were measured using enzyme-linked immunosorbent assay (ELISA) kits. Protein expression of Phosphorylated p38/p38 was determined using western blots. We found that HNG treatment attenuated the STZ-induced myocardial hypertrophy and significantly improved heart function. Also, its treatment proved effective as it reduced the levels of several myocardial injury indicators, including creatine kinase-MB (CK-MB), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and both the cardiac and plasma levels of TNF-α and IL-6, highlighting its effect on the STZ-induced myocardial injury. Lastly, HNG suppressed the activation of the p38/nuclear factor kappa-B (NF-κB) signaling pathway. S14G humanin possesses protective effects against streptozotocin-induced cardiac dysfunction through inhibiting the activation of the p38/NF-κB signaling pathway. Taylor & Francis 2021-09-10 /pmc/articles/PMC8806847/ /pubmed/34506248 http://dx.doi.org/10.1080/21655979.2021.1964894 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
Chen, Xiaopan
Yun, Chuan
Zheng, Hailong
Chen, Xu
Han, Qianfei
Pan, Hua
Wang, Yang
Zhong, Jianghua
The protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunction
title The protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunction
title_full The protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunction
title_fullStr The protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunction
title_full_unstemmed The protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunction
title_short The protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunction
title_sort protective effects of s14g-humanin (hng) against streptozotocin (stz)-induced cardiac dysfunction
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806847/
https://www.ncbi.nlm.nih.gov/pubmed/34506248
http://dx.doi.org/10.1080/21655979.2021.1964894
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