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Intracoronary application of nicorandil regulates the inflammatory response induced by percutaneous coronary intervention
Intracoronary application of nicorandil can effectively reduce the myocardial no‐reflow (MNR) after percutaneous coronary intervention (PCI). We sought to investigate the mechanisms of nicorandil in preventing MNR, besides that of dilating the coronary microvasculature. A total of 60 patients underg...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7176882/ https://www.ncbi.nlm.nih.gov/pubmed/32175662 http://dx.doi.org/10.1111/jcmm.15169 |
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author | Hu, Keqing Wang, Xiaoqi Hu, Hongyan Xu, Zhongyang Zhang, Jiaxing An, Guipeng Su, Guohai |
author_facet | Hu, Keqing Wang, Xiaoqi Hu, Hongyan Xu, Zhongyang Zhang, Jiaxing An, Guipeng Su, Guohai |
author_sort | Hu, Keqing |
collection | PubMed |
description | Intracoronary application of nicorandil can effectively reduce the myocardial no‐reflow (MNR) after percutaneous coronary intervention (PCI). We sought to investigate the mechanisms of nicorandil in preventing MNR, besides that of dilating the coronary microvasculature. A total of 60 patients undergoing PCI were enrolled and randomly divided into a nicorandil group and a control group. Before PCI, 2 mg of nicorandil or an equal volume of normal saline was injected into the coronary artery. Blood samples were collected before, 24 hours and 1 week after PCI and inflammatory cytokines were tested. In the control group, the expression of pro‐inflammatory cytokines was significantly increased, while the anti‐inflammatory cytokines were decreased 24 hours after PCI. In contrast, these changes were reversed in the nicorandil group, indicating that nicorandil regulated the inflammatory response induced by PCI. Then, proteomic analysis was performed to further elucidate the potential mechanisms. A total of 53 differentially expressed proteins (DEPs) were found 24 hours after PCI in the control group, and the changes of these relevant genes were reversed in the nicorandil group. These DEPs were significantly enriched in the inflammatory pathways. In conclusion, the intracoronary application of nicorandil before PCI can regulate the inflammatory responses induced by PCI, which might be an important mechanism of nicorandil in preventing MNR. |
format | Online Article Text |
id | pubmed-7176882 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-71768822020-04-24 Intracoronary application of nicorandil regulates the inflammatory response induced by percutaneous coronary intervention Hu, Keqing Wang, Xiaoqi Hu, Hongyan Xu, Zhongyang Zhang, Jiaxing An, Guipeng Su, Guohai J Cell Mol Med Original Articles Intracoronary application of nicorandil can effectively reduce the myocardial no‐reflow (MNR) after percutaneous coronary intervention (PCI). We sought to investigate the mechanisms of nicorandil in preventing MNR, besides that of dilating the coronary microvasculature. A total of 60 patients undergoing PCI were enrolled and randomly divided into a nicorandil group and a control group. Before PCI, 2 mg of nicorandil or an equal volume of normal saline was injected into the coronary artery. Blood samples were collected before, 24 hours and 1 week after PCI and inflammatory cytokines were tested. In the control group, the expression of pro‐inflammatory cytokines was significantly increased, while the anti‐inflammatory cytokines were decreased 24 hours after PCI. In contrast, these changes were reversed in the nicorandil group, indicating that nicorandil regulated the inflammatory response induced by PCI. Then, proteomic analysis was performed to further elucidate the potential mechanisms. A total of 53 differentially expressed proteins (DEPs) were found 24 hours after PCI in the control group, and the changes of these relevant genes were reversed in the nicorandil group. These DEPs were significantly enriched in the inflammatory pathways. In conclusion, the intracoronary application of nicorandil before PCI can regulate the inflammatory responses induced by PCI, which might be an important mechanism of nicorandil in preventing MNR. John Wiley and Sons Inc. 2020-03-16 2020-04 /pmc/articles/PMC7176882/ /pubmed/32175662 http://dx.doi.org/10.1111/jcmm.15169 Text en © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Hu, Keqing Wang, Xiaoqi Hu, Hongyan Xu, Zhongyang Zhang, Jiaxing An, Guipeng Su, Guohai Intracoronary application of nicorandil regulates the inflammatory response induced by percutaneous coronary intervention |
title | Intracoronary application of nicorandil regulates the inflammatory response induced by percutaneous coronary intervention |
title_full | Intracoronary application of nicorandil regulates the inflammatory response induced by percutaneous coronary intervention |
title_fullStr | Intracoronary application of nicorandil regulates the inflammatory response induced by percutaneous coronary intervention |
title_full_unstemmed | Intracoronary application of nicorandil regulates the inflammatory response induced by percutaneous coronary intervention |
title_short | Intracoronary application of nicorandil regulates the inflammatory response induced by percutaneous coronary intervention |
title_sort | intracoronary application of nicorandil regulates the inflammatory response induced by percutaneous coronary intervention |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7176882/ https://www.ncbi.nlm.nih.gov/pubmed/32175662 http://dx.doi.org/10.1111/jcmm.15169 |
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