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Reynoutrin Improves Ischemic Heart Failure in Rats Via Targeting S100A1

This study investigated the effects of reynoutrin on the improvement of ischemic heart failure (IHF) and its possible mechanism in rats. The rat heart failure model was established by permanently ligating the left anterior descending coronary artery (LAD) and administering different doses of reynout...

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Autores principales: Yang, Wenkai, Tu, Hanjian, Tang, Kai, Huang, Haozhong, Ou, Shi, Wu, Jianguo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8343003/
https://www.ncbi.nlm.nih.gov/pubmed/34366855
http://dx.doi.org/10.3389/fphar.2021.703962
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author Yang, Wenkai
Tu, Hanjian
Tang, Kai
Huang, Haozhong
Ou, Shi
Wu, Jianguo
author_facet Yang, Wenkai
Tu, Hanjian
Tang, Kai
Huang, Haozhong
Ou, Shi
Wu, Jianguo
author_sort Yang, Wenkai
collection PubMed
description This study investigated the effects of reynoutrin on the improvement of ischemic heart failure (IHF) and its possible mechanism in rats. The rat heart failure model was established by permanently ligating the left anterior descending coronary artery (LAD) and administering different doses of reynoutrin. Cardiac function, inflammatory factors releasing, oxidative stress, cardiomyocytes apoptosis, and myocardial fibrosis were evaluated. Western blotting was used to determine protein expression levels of S100 calcium-binding protein A1 (S100A1), matrix metallopeptidase 2(MMP2), MMP9, phosphorylated (p-) p65, and transforming growth factor -β1 (TGF-β1) in myocardial tissue of the left ventricle. Results showed that reynoutrin significantly improved cardiac function, suppressed the release of inflammatory factors, reduced oxidative stress, inhibited cardiomyocytes apoptosis, and attenuated myocardial fibrosis in rats with IHF. In rat myocardial tissue, permanent LAD-ligation resulted in a significant down-regulation in S100A1 expression, whereas reynoutrin significantly up-regulated S100A1 protein expression while down-regulating MMP2, MMP9, p-p65, and TGF-β1 expressions. However, when S100A1 was knocked down in myocardial tissue, the above-mentioned positive effects of reynoutrin were significantly reversed. Reynoutrin is a potential natural drug for the treatment of IHF, and its mechanism of action involves the up-regulation of S100A1 expression, thereby inhibiting expressions of MMPs and the transcriptional activity of nuclear factor kappa-B.
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spelling pubmed-83430032021-08-07 Reynoutrin Improves Ischemic Heart Failure in Rats Via Targeting S100A1 Yang, Wenkai Tu, Hanjian Tang, Kai Huang, Haozhong Ou, Shi Wu, Jianguo Front Pharmacol Pharmacology This study investigated the effects of reynoutrin on the improvement of ischemic heart failure (IHF) and its possible mechanism in rats. The rat heart failure model was established by permanently ligating the left anterior descending coronary artery (LAD) and administering different doses of reynoutrin. Cardiac function, inflammatory factors releasing, oxidative stress, cardiomyocytes apoptosis, and myocardial fibrosis were evaluated. Western blotting was used to determine protein expression levels of S100 calcium-binding protein A1 (S100A1), matrix metallopeptidase 2(MMP2), MMP9, phosphorylated (p-) p65, and transforming growth factor -β1 (TGF-β1) in myocardial tissue of the left ventricle. Results showed that reynoutrin significantly improved cardiac function, suppressed the release of inflammatory factors, reduced oxidative stress, inhibited cardiomyocytes apoptosis, and attenuated myocardial fibrosis in rats with IHF. In rat myocardial tissue, permanent LAD-ligation resulted in a significant down-regulation in S100A1 expression, whereas reynoutrin significantly up-regulated S100A1 protein expression while down-regulating MMP2, MMP9, p-p65, and TGF-β1 expressions. However, when S100A1 was knocked down in myocardial tissue, the above-mentioned positive effects of reynoutrin were significantly reversed. Reynoutrin is a potential natural drug for the treatment of IHF, and its mechanism of action involves the up-regulation of S100A1 expression, thereby inhibiting expressions of MMPs and the transcriptional activity of nuclear factor kappa-B. Frontiers Media S.A. 2021-07-23 /pmc/articles/PMC8343003/ /pubmed/34366855 http://dx.doi.org/10.3389/fphar.2021.703962 Text en Copyright © 2021 Yang, Tu, Tang, Huang, Ou and Wu. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Yang, Wenkai
Tu, Hanjian
Tang, Kai
Huang, Haozhong
Ou, Shi
Wu, Jianguo
Reynoutrin Improves Ischemic Heart Failure in Rats Via Targeting S100A1
title Reynoutrin Improves Ischemic Heart Failure in Rats Via Targeting S100A1
title_full Reynoutrin Improves Ischemic Heart Failure in Rats Via Targeting S100A1
title_fullStr Reynoutrin Improves Ischemic Heart Failure in Rats Via Targeting S100A1
title_full_unstemmed Reynoutrin Improves Ischemic Heart Failure in Rats Via Targeting S100A1
title_short Reynoutrin Improves Ischemic Heart Failure in Rats Via Targeting S100A1
title_sort reynoutrin improves ischemic heart failure in rats via targeting s100a1
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8343003/
https://www.ncbi.nlm.nih.gov/pubmed/34366855
http://dx.doi.org/10.3389/fphar.2021.703962
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