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Niacin Modulates Pro-inflammatory Cytokine Secretion. A Potential Mechanism Involved in its Anti-atherosclerotic Effect

The pathogenesis of atherosclerosis includes the assignment of a critical role to cells of the monocyte/macrophage lineage and to pro-inflammatory cytokines. Niacin is known to improve lipid metabolism and to produce beneficial modification of cardiovascular risk factors. The aim of this work was to...

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Autores principales: Lipszyc, Pedro Saul, Cremaschi, Graciela Alicia, Zubilete, María Zorrilla, Bertolino, Maria Laura Aón, Capani, Francisco, Genaro, Ana Maria, Wald, Miriam Ruth
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bentham Open 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3805984/
https://www.ncbi.nlm.nih.gov/pubmed/24155799
http://dx.doi.org/10.2174/1874192401307010090
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author Lipszyc, Pedro Saul
Cremaschi, Graciela Alicia
Zubilete, María Zorrilla
Bertolino, Maria Laura Aón
Capani, Francisco
Genaro, Ana Maria
Wald, Miriam Ruth
author_facet Lipszyc, Pedro Saul
Cremaschi, Graciela Alicia
Zubilete, María Zorrilla
Bertolino, Maria Laura Aón
Capani, Francisco
Genaro, Ana Maria
Wald, Miriam Ruth
author_sort Lipszyc, Pedro Saul
collection PubMed
description The pathogenesis of atherosclerosis includes the assignment of a critical role to cells of the monocyte/macrophage lineage and to pro-inflammatory cytokines. Niacin is known to improve lipid metabolism and to produce beneficial modification of cardiovascular risk factors. The aim of this work was to investigate if Niacin is able to modulate pro-inflammatory cytokine production in macrophages in a murine model of atherosclerosis. For this purpose C57Bl/6J mice fed with atherogenic diet (AGD) or with conventional chow diet were used. The AGD group showed an increase in body weight and in total plasma cholesterol, with no differences in triglyceride or HDL levels. Lesions in arterial walls were observed. The characterization of Niacin receptor showed an increase in the receptor number of macrophages from the AGD group. Macrophages from control and AGD animals treated in vitro with an inflammatory stimulus showed elevated levels of IL-6, IL-1 and TNF-α, that were even higher in macrophages from AGD mice. Niacin was able to decrease the production of pro-inflammatory cytokines in stimulated macrophages. Similar effect of Niacin was observed in an in vivo model of inflammation. These results show an attenuating inflammatory mechanism for this therapeutic agent and would point out its potential action in plaque stabilization and in the prevention of atherosclerosis progression. Furthermore, the present results provide the basis for future studies on the potential contribution of Niacin to anti-inflammatory therapies.
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spelling pubmed-38059842013-10-23 Niacin Modulates Pro-inflammatory Cytokine Secretion. A Potential Mechanism Involved in its Anti-atherosclerotic Effect Lipszyc, Pedro Saul Cremaschi, Graciela Alicia Zubilete, María Zorrilla Bertolino, Maria Laura Aón Capani, Francisco Genaro, Ana Maria Wald, Miriam Ruth Open Cardiovasc Med J Article The pathogenesis of atherosclerosis includes the assignment of a critical role to cells of the monocyte/macrophage lineage and to pro-inflammatory cytokines. Niacin is known to improve lipid metabolism and to produce beneficial modification of cardiovascular risk factors. The aim of this work was to investigate if Niacin is able to modulate pro-inflammatory cytokine production in macrophages in a murine model of atherosclerosis. For this purpose C57Bl/6J mice fed with atherogenic diet (AGD) or with conventional chow diet were used. The AGD group showed an increase in body weight and in total plasma cholesterol, with no differences in triglyceride or HDL levels. Lesions in arterial walls were observed. The characterization of Niacin receptor showed an increase in the receptor number of macrophages from the AGD group. Macrophages from control and AGD animals treated in vitro with an inflammatory stimulus showed elevated levels of IL-6, IL-1 and TNF-α, that were even higher in macrophages from AGD mice. Niacin was able to decrease the production of pro-inflammatory cytokines in stimulated macrophages. Similar effect of Niacin was observed in an in vivo model of inflammation. These results show an attenuating inflammatory mechanism for this therapeutic agent and would point out its potential action in plaque stabilization and in the prevention of atherosclerosis progression. Furthermore, the present results provide the basis for future studies on the potential contribution of Niacin to anti-inflammatory therapies. Bentham Open 2013-09-20 /pmc/articles/PMC3805984/ /pubmed/24155799 http://dx.doi.org/10.2174/1874192401307010090 Text en © Lipszyc et al.; Licensee Bentham Open. http://creativecommons.org/licenses/by-nc/3.0/ This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
spellingShingle Article
Lipszyc, Pedro Saul
Cremaschi, Graciela Alicia
Zubilete, María Zorrilla
Bertolino, Maria Laura Aón
Capani, Francisco
Genaro, Ana Maria
Wald, Miriam Ruth
Niacin Modulates Pro-inflammatory Cytokine Secretion. A Potential Mechanism Involved in its Anti-atherosclerotic Effect
title Niacin Modulates Pro-inflammatory Cytokine Secretion. A Potential Mechanism Involved in its Anti-atherosclerotic Effect
title_full Niacin Modulates Pro-inflammatory Cytokine Secretion. A Potential Mechanism Involved in its Anti-atherosclerotic Effect
title_fullStr Niacin Modulates Pro-inflammatory Cytokine Secretion. A Potential Mechanism Involved in its Anti-atherosclerotic Effect
title_full_unstemmed Niacin Modulates Pro-inflammatory Cytokine Secretion. A Potential Mechanism Involved in its Anti-atherosclerotic Effect
title_short Niacin Modulates Pro-inflammatory Cytokine Secretion. A Potential Mechanism Involved in its Anti-atherosclerotic Effect
title_sort niacin modulates pro-inflammatory cytokine secretion. a potential mechanism involved in its anti-atherosclerotic effect
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3805984/
https://www.ncbi.nlm.nih.gov/pubmed/24155799
http://dx.doi.org/10.2174/1874192401307010090
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