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Urolithin B, a Gut Microbiota Metabolite, Reduced Susceptibility to Myocardial Arrhythmic Predisposition after Hypoxia
Cardiomyocyte apoptosis, neural remodeling, and gap junction channel change play critical roles in ventricular arrhythmia (VA) after acute myocardial infarction (AMI). Urolithin B (UB), one of the gut metabolites of ellagitannins, a class of antioxidant polyphenols, has various biological activities...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8847032/ https://www.ncbi.nlm.nih.gov/pubmed/35178131 http://dx.doi.org/10.1155/2022/6517266 |
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author | Huang, Xin Gao, Hong Jiang, Xiaojie Zheng, Zeqi |
author_facet | Huang, Xin Gao, Hong Jiang, Xiaojie Zheng, Zeqi |
author_sort | Huang, Xin |
collection | PubMed |
description | Cardiomyocyte apoptosis, neural remodeling, and gap junction channel change play critical roles in ventricular arrhythmia (VA) after acute myocardial infarction (AMI). Urolithin B (UB), one of the gut metabolites of ellagitannins, a class of antioxidant polyphenols, has various biological activities, but its direct role in cardiomyocyte apoptosis, neural remodeling, and gap junction channel change after AMI remains elusive. We investigated whether urolithin B reduced susceptibility of myocardial arrhythmic after myocardial infarction (MI). In vitro, the cardiomyocytes were subjected to hypoxia (94% N(2)/5% CO(2)/1% O(2)) for 3 hours. Cardiomyocyte apoptosis was assessed by TUNEL staining and western blotting. Urolithin B was found to decrease the number of apoptotic cells after hypoxia. Moreover, there was a substantial decrease in the expression of neural remodeling markers in the urolithin B treatment group. Urolithin B significantly increased the expression level of gap junction channel protein. Mechanistically, urolithin B inhibited cardiomyocyte apoptosis by activating Akt/the mammalian target of rapamycin (mTOR) pathway, and the protection of urolithin B against cardiomyocyte apoptosis was compromised with Akt gene silencing. Furthermore, urolithin B suppressed nuclear translocation of nuclear factor-kB (NF-κB) to facilitate nerve remodeling. Taken together, our findings suggested that UB reduced the occurrence of myocardial arrhythmias after hypoxia via regulation of the Akt/mTOR pathway and NF-κB nuclear translocation, which highlights the potential of UB as a novel therapy for ischemic heart disease. |
format | Online Article Text |
id | pubmed-8847032 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-88470322022-02-16 Urolithin B, a Gut Microbiota Metabolite, Reduced Susceptibility to Myocardial Arrhythmic Predisposition after Hypoxia Huang, Xin Gao, Hong Jiang, Xiaojie Zheng, Zeqi Dis Markers Research Article Cardiomyocyte apoptosis, neural remodeling, and gap junction channel change play critical roles in ventricular arrhythmia (VA) after acute myocardial infarction (AMI). Urolithin B (UB), one of the gut metabolites of ellagitannins, a class of antioxidant polyphenols, has various biological activities, but its direct role in cardiomyocyte apoptosis, neural remodeling, and gap junction channel change after AMI remains elusive. We investigated whether urolithin B reduced susceptibility of myocardial arrhythmic after myocardial infarction (MI). In vitro, the cardiomyocytes were subjected to hypoxia (94% N(2)/5% CO(2)/1% O(2)) for 3 hours. Cardiomyocyte apoptosis was assessed by TUNEL staining and western blotting. Urolithin B was found to decrease the number of apoptotic cells after hypoxia. Moreover, there was a substantial decrease in the expression of neural remodeling markers in the urolithin B treatment group. Urolithin B significantly increased the expression level of gap junction channel protein. Mechanistically, urolithin B inhibited cardiomyocyte apoptosis by activating Akt/the mammalian target of rapamycin (mTOR) pathway, and the protection of urolithin B against cardiomyocyte apoptosis was compromised with Akt gene silencing. Furthermore, urolithin B suppressed nuclear translocation of nuclear factor-kB (NF-κB) to facilitate nerve remodeling. Taken together, our findings suggested that UB reduced the occurrence of myocardial arrhythmias after hypoxia via regulation of the Akt/mTOR pathway and NF-κB nuclear translocation, which highlights the potential of UB as a novel therapy for ischemic heart disease. Hindawi 2022-02-08 /pmc/articles/PMC8847032/ /pubmed/35178131 http://dx.doi.org/10.1155/2022/6517266 Text en Copyright © 2022 Xin Huang et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Huang, Xin Gao, Hong Jiang, Xiaojie Zheng, Zeqi Urolithin B, a Gut Microbiota Metabolite, Reduced Susceptibility to Myocardial Arrhythmic Predisposition after Hypoxia |
title | Urolithin B, a Gut Microbiota Metabolite, Reduced Susceptibility to Myocardial Arrhythmic Predisposition after Hypoxia |
title_full | Urolithin B, a Gut Microbiota Metabolite, Reduced Susceptibility to Myocardial Arrhythmic Predisposition after Hypoxia |
title_fullStr | Urolithin B, a Gut Microbiota Metabolite, Reduced Susceptibility to Myocardial Arrhythmic Predisposition after Hypoxia |
title_full_unstemmed | Urolithin B, a Gut Microbiota Metabolite, Reduced Susceptibility to Myocardial Arrhythmic Predisposition after Hypoxia |
title_short | Urolithin B, a Gut Microbiota Metabolite, Reduced Susceptibility to Myocardial Arrhythmic Predisposition after Hypoxia |
title_sort | urolithin b, a gut microbiota metabolite, reduced susceptibility to myocardial arrhythmic predisposition after hypoxia |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8847032/ https://www.ncbi.nlm.nih.gov/pubmed/35178131 http://dx.doi.org/10.1155/2022/6517266 |
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