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Suppression of NF-κB Reduces Myocardial No-Reflow
No-reflow phenomenon is a risk factor which severely compromises the benefits of coronary revascularization in patients with acute myocardial infarction. Inflammatory response, as an essential component of cardiac ischemia/reperfusion (I/R) injury, has been suggested to contribute to the myocardial...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3467223/ https://www.ncbi.nlm.nih.gov/pubmed/23056624 http://dx.doi.org/10.1371/journal.pone.0047306 |
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author | Zeng, Min Yan, Hongbing Chen, Yi Zhao, Han-jun Lv, Yuan Liu, Cheng Zhou, Peng Zhao, Bo |
author_facet | Zeng, Min Yan, Hongbing Chen, Yi Zhao, Han-jun Lv, Yuan Liu, Cheng Zhou, Peng Zhao, Bo |
author_sort | Zeng, Min |
collection | PubMed |
description | No-reflow phenomenon is a risk factor which severely compromises the benefits of coronary revascularization in patients with acute myocardial infarction. Inflammatory response, as an essential component of cardiac ischemia/reperfusion (I/R) injury, has been suggested to contribute to the myocardial no-reflow. Since nuclear factor kappa B (NF-κB) is a key mediator of inflammation, we reasoned that inhibition of NF-κB might reduce the extent of no-reflow. To test this hypothesis, the left circumflex coronary arteries of New Zealand white male rabbits were ligated for 1.5 h, followed by reperfusion for 1 h to induce I/R injury. Pretreatment of the rabbits with a specific NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), significantly attenuated neutrophil infiltration in the no-reflow area as well as the expansion of no-reflow. These beneficial effects were associated with a marked reduction in the serum levels of myocardial induced I/R tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), and CXCL16. Consistently, simulative I/R culture of human umbilical vein endothelial cells (HUVECs) resulted in an increase of TNF-α, ICAM-1 and CXCL16, and all of these changes were significantly suppressed by pretreatment of the cells with PDTC or with siRNA-mediated p65 knockdown. Our data thus suggest that inhibition of NF-κB may reduce I/R-associated myocardial no-reflow through reduction of myocardial inflammation. |
format | Online Article Text |
id | pubmed-3467223 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-34672232012-10-10 Suppression of NF-κB Reduces Myocardial No-Reflow Zeng, Min Yan, Hongbing Chen, Yi Zhao, Han-jun Lv, Yuan Liu, Cheng Zhou, Peng Zhao, Bo PLoS One Research Article No-reflow phenomenon is a risk factor which severely compromises the benefits of coronary revascularization in patients with acute myocardial infarction. Inflammatory response, as an essential component of cardiac ischemia/reperfusion (I/R) injury, has been suggested to contribute to the myocardial no-reflow. Since nuclear factor kappa B (NF-κB) is a key mediator of inflammation, we reasoned that inhibition of NF-κB might reduce the extent of no-reflow. To test this hypothesis, the left circumflex coronary arteries of New Zealand white male rabbits were ligated for 1.5 h, followed by reperfusion for 1 h to induce I/R injury. Pretreatment of the rabbits with a specific NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), significantly attenuated neutrophil infiltration in the no-reflow area as well as the expansion of no-reflow. These beneficial effects were associated with a marked reduction in the serum levels of myocardial induced I/R tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), and CXCL16. Consistently, simulative I/R culture of human umbilical vein endothelial cells (HUVECs) resulted in an increase of TNF-α, ICAM-1 and CXCL16, and all of these changes were significantly suppressed by pretreatment of the cells with PDTC or with siRNA-mediated p65 knockdown. Our data thus suggest that inhibition of NF-κB may reduce I/R-associated myocardial no-reflow through reduction of myocardial inflammation. Public Library of Science 2012-10-09 /pmc/articles/PMC3467223/ /pubmed/23056624 http://dx.doi.org/10.1371/journal.pone.0047306 Text en © 2012 Zeng et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited. |
spellingShingle | Research Article Zeng, Min Yan, Hongbing Chen, Yi Zhao, Han-jun Lv, Yuan Liu, Cheng Zhou, Peng Zhao, Bo Suppression of NF-κB Reduces Myocardial No-Reflow |
title | Suppression of NF-κB Reduces Myocardial No-Reflow |
title_full | Suppression of NF-κB Reduces Myocardial No-Reflow |
title_fullStr | Suppression of NF-κB Reduces Myocardial No-Reflow |
title_full_unstemmed | Suppression of NF-κB Reduces Myocardial No-Reflow |
title_short | Suppression of NF-κB Reduces Myocardial No-Reflow |
title_sort | suppression of nf-κb reduces myocardial no-reflow |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3467223/ https://www.ncbi.nlm.nih.gov/pubmed/23056624 http://dx.doi.org/10.1371/journal.pone.0047306 |
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