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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Main Authors: Xiaopan Chen, Chuan Yun, Hailong Zheng, Xu Chen, Qianfei Han, Hua Pan, Yang Wang, Jianghua Zhong
Format: Article
Language:English
Published: Taylor & Francis Group 2021-01-01
Series:Bioengineered
Subjects:
Online Access:http://dx.doi.org/10.1080/21655979.2021.1964894
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author Xiaopan Chen
Chuan Yun
Hailong Zheng
Xu Chen
Qianfei Han
Hua Pan
Yang Wang
Jianghua Zhong
author_facet Xiaopan Chen
Chuan Yun
Hailong Zheng
Xu Chen
Qianfei Han
Hua Pan
Yang Wang
Jianghua Zhong
author_sort Xiaopan Chen
collection DOAJ
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 doaj.art-cdd72acc42764332af938cf6ddd69f2b2022-12-22T04:04:18ZengTaylor & Francis GroupBioengineered2165-59792165-59872021-01-011215491550310.1080/21655979.2021.19648941964894The protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunctionXiaopan Chen0Chuan Yun1Hailong Zheng2Xu Chen3Qianfei Han4Hua Pan5Yang Wang6Jianghua Zhong7The First Affiliated Hospital of Hainan Medical UniversityThe First Affiliated Hospital of Hainan Medical UniversityThe First Affiliated Hospital of Hainan Medical UniversityThe First Affiliated Hospital of Hainan Medical UniversityThe First Affiliated Hospital of Hainan Medical UniversityThe First Affiliated Hospital of Hainan Medical UniversityAffiliated Haikou Hospital Of Xiangya Medical College, Central South UniversityAffiliated Haikou Hospital Of Xiangya Medical College, Central South UniversityExcessive 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.http://dx.doi.org/10.1080/21655979.2021.1964894s14g-humaninstreptozotocincardiac dysfunctiondiabetes
spellingShingle Xiaopan Chen
Chuan Yun
Hailong Zheng
Xu Chen
Qianfei Han
Hua Pan
Yang Wang
Jianghua Zhong
The protective effects of S14G-humanin (HNG) against streptozotocin (STZ)-induced cardiac dysfunction
Bioengineered
s14g-humanin
streptozotocin
cardiac dysfunction
diabetes
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 s14g-humanin
streptozotocin
cardiac dysfunction
diabetes
url http://dx.doi.org/10.1080/21655979.2021.1964894
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