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Astragalus polysaccharides protect cardiac stem and progenitor cells by the inhibition of oxidative stress-mediated apoptosis in diabetic hearts

INTRODUCTION: Diabetic cardiomyopathy is characterized by an imbalance between myocyte death and regeneration mediated by the progressive loss of cardiac stem and progenitor cells (CSPCs) by apoptosis and necrosis due to the activation of oxidative stress with diabetes. In this study, we evaluated t...

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Autores principales: Chen, Wei, Ju, Jing, Yang, Yehong, Wang, Hao, Chen, Wenjie, Zhao, Xuelan, Ye, Hongying, Zhang, Yu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5916262/
https://www.ncbi.nlm.nih.gov/pubmed/29719380
http://dx.doi.org/10.2147/DDDT.S155686
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author Chen, Wei
Ju, Jing
Yang, Yehong
Wang, Hao
Chen, Wenjie
Zhao, Xuelan
Ye, Hongying
Zhang, Yu
author_facet Chen, Wei
Ju, Jing
Yang, Yehong
Wang, Hao
Chen, Wenjie
Zhao, Xuelan
Ye, Hongying
Zhang, Yu
author_sort Chen, Wei
collection PubMed
description INTRODUCTION: Diabetic cardiomyopathy is characterized by an imbalance between myocyte death and regeneration mediated by the progressive loss of cardiac stem and progenitor cells (CSPCs) by apoptosis and necrosis due to the activation of oxidative stress with diabetes. In this study, we evaluated the beneficial effect of astragalus polysaccharides (APS) therapy on the protection of CSPCs through its antioxidative capacity in diabetic hearts. MATERIALS AND METHODS: Streptozotocin (STZ)-induced diabetic mice and heterozygous (SOD2+/−) knockout mice were employed and administered with APS. Ventricular CSPCs were isolated for oxidative evaluation. The abundance, apoptosis and proliferation, reactive oxygen species (ROS) formation, oxidative damage, and SOD2 protein levels and activities were evaluated in ventricular CSPCs. RESULTS: We confirmed that APS increased the CSPC abundance, reduced the apoptosis of CSPCs, and enhanced the proliferation of CSPCs in both STZ-induced diabetic mice and nondiabetic SOD2+/− mice. In addition, therapy of APS enhanced SOD2 protein levels and enzyme activities, and inhibited ROS formation and oxidative damage of CSPCs from both STZ-induced diabetic mice and nondiabetic SOD2+/− mice. CONCLUSION: Our findings demonstrated the positive effect of APS on the rescue of CSPC preservation in diabetes, dependent on the inhibition of oxidative stress-mediated apoptosis.
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spelling pubmed-59162622018-05-01 Astragalus polysaccharides protect cardiac stem and progenitor cells by the inhibition of oxidative stress-mediated apoptosis in diabetic hearts Chen, Wei Ju, Jing Yang, Yehong Wang, Hao Chen, Wenjie Zhao, Xuelan Ye, Hongying Zhang, Yu Drug Des Devel Ther Original Research INTRODUCTION: Diabetic cardiomyopathy is characterized by an imbalance between myocyte death and regeneration mediated by the progressive loss of cardiac stem and progenitor cells (CSPCs) by apoptosis and necrosis due to the activation of oxidative stress with diabetes. In this study, we evaluated the beneficial effect of astragalus polysaccharides (APS) therapy on the protection of CSPCs through its antioxidative capacity in diabetic hearts. MATERIALS AND METHODS: Streptozotocin (STZ)-induced diabetic mice and heterozygous (SOD2+/−) knockout mice were employed and administered with APS. Ventricular CSPCs were isolated for oxidative evaluation. The abundance, apoptosis and proliferation, reactive oxygen species (ROS) formation, oxidative damage, and SOD2 protein levels and activities were evaluated in ventricular CSPCs. RESULTS: We confirmed that APS increased the CSPC abundance, reduced the apoptosis of CSPCs, and enhanced the proliferation of CSPCs in both STZ-induced diabetic mice and nondiabetic SOD2+/− mice. In addition, therapy of APS enhanced SOD2 protein levels and enzyme activities, and inhibited ROS formation and oxidative damage of CSPCs from both STZ-induced diabetic mice and nondiabetic SOD2+/− mice. CONCLUSION: Our findings demonstrated the positive effect of APS on the rescue of CSPC preservation in diabetes, dependent on the inhibition of oxidative stress-mediated apoptosis. Dove Medical Press 2018-04-20 /pmc/articles/PMC5916262/ /pubmed/29719380 http://dx.doi.org/10.2147/DDDT.S155686 Text en © 2018 Chen et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Chen, Wei
Ju, Jing
Yang, Yehong
Wang, Hao
Chen, Wenjie
Zhao, Xuelan
Ye, Hongying
Zhang, Yu
Astragalus polysaccharides protect cardiac stem and progenitor cells by the inhibition of oxidative stress-mediated apoptosis in diabetic hearts
title Astragalus polysaccharides protect cardiac stem and progenitor cells by the inhibition of oxidative stress-mediated apoptosis in diabetic hearts
title_full Astragalus polysaccharides protect cardiac stem and progenitor cells by the inhibition of oxidative stress-mediated apoptosis in diabetic hearts
title_fullStr Astragalus polysaccharides protect cardiac stem and progenitor cells by the inhibition of oxidative stress-mediated apoptosis in diabetic hearts
title_full_unstemmed Astragalus polysaccharides protect cardiac stem and progenitor cells by the inhibition of oxidative stress-mediated apoptosis in diabetic hearts
title_short Astragalus polysaccharides protect cardiac stem and progenitor cells by the inhibition of oxidative stress-mediated apoptosis in diabetic hearts
title_sort astragalus polysaccharides protect cardiac stem and progenitor cells by the inhibition of oxidative stress-mediated apoptosis in diabetic hearts
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5916262/
https://www.ncbi.nlm.nih.gov/pubmed/29719380
http://dx.doi.org/10.2147/DDDT.S155686
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