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Effect of n-3 fatty acids on the expression of inflammatory genes in THP-1 macrophages

BACKGROUND: Uncontrolled inflammation participates in the development of inflammatory diseases. Beneficial effects of polyunsaturated fatty acids belonging to the n-3 family such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on inflammation have been reported. The present study inves...

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Autores principales: Allam-Ndoul, Bénédicte, Guénard, Frédéric, Barbier, Olivier, Vohl, Marie-Claude
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4820929/
https://www.ncbi.nlm.nih.gov/pubmed/27044314
http://dx.doi.org/10.1186/s12944-016-0241-4
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author Allam-Ndoul, Bénédicte
Guénard, Frédéric
Barbier, Olivier
Vohl, Marie-Claude
author_facet Allam-Ndoul, Bénédicte
Guénard, Frédéric
Barbier, Olivier
Vohl, Marie-Claude
author_sort Allam-Ndoul, Bénédicte
collection PubMed
description BACKGROUND: Uncontrolled inflammation participates in the development of inflammatory diseases. Beneficial effects of polyunsaturated fatty acids belonging to the n-3 family such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on inflammation have been reported. The present study investigates the basal effects of EPA, DHA and a mixture EPA + DHA on the expression of 10 genes (AKT1, MAPK, NFKB, TNFA, IL1Β, MCP1, ALOX5, PTGS2, MGST1and NOS2) related to inflammation in unstimulated cultured THP1 macrophages. Cells were incubated for 24 h with n-3 PUFAs (50 μM and 10 μM EPA, DHA, EPA + DHA). Expression levels of inflammatory genes were analyzed by real-time PCR. RESULTS: 50 μM, 10 μM EPA and 50 μM EPA + DHA decreased the expression of genes involved in the NF-κB pathway (MAPK, AKT1, and NFKB). Treatment with 50 μM, 10 μM EPA, 50 μM DHA and EPA + DHA decreased expression levels of cytokines genes IL1Β and MCP1. TNFA expression was decreased by 50 μM, 10 μM of EPA, DHA and with 50 μM EPA + DHA. Two genes involved in the fatty acid metabolism (PTGS2 and ALOX5) were also modulated by the n-3 FAs. 50 μM of DHA and EPA + DHA inhibited PTGS2 expression when the two concentrations of EPA, 50 μM DHA and EPA + DHA inhibited ALOX5 expression. Finally, the effects of n-3 FAs were studied among genes involved in the oxidative stress. 50 μM of each fatty acid increased MGST1 expression. Both concentration of EPA and 50 μM DHA decreased NOS2 expression. CONCLUSION: EPA seems to be more effective than DHA and EPA + DHA in modulating expression levels of selected inflammatory genes. The concentration of 50 μM was globally more effective than 10 μM.
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spelling pubmed-48209292016-04-06 Effect of n-3 fatty acids on the expression of inflammatory genes in THP-1 macrophages Allam-Ndoul, Bénédicte Guénard, Frédéric Barbier, Olivier Vohl, Marie-Claude Lipids Health Dis Research BACKGROUND: Uncontrolled inflammation participates in the development of inflammatory diseases. Beneficial effects of polyunsaturated fatty acids belonging to the n-3 family such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on inflammation have been reported. The present study investigates the basal effects of EPA, DHA and a mixture EPA + DHA on the expression of 10 genes (AKT1, MAPK, NFKB, TNFA, IL1Β, MCP1, ALOX5, PTGS2, MGST1and NOS2) related to inflammation in unstimulated cultured THP1 macrophages. Cells were incubated for 24 h with n-3 PUFAs (50 μM and 10 μM EPA, DHA, EPA + DHA). Expression levels of inflammatory genes were analyzed by real-time PCR. RESULTS: 50 μM, 10 μM EPA and 50 μM EPA + DHA decreased the expression of genes involved in the NF-κB pathway (MAPK, AKT1, and NFKB). Treatment with 50 μM, 10 μM EPA, 50 μM DHA and EPA + DHA decreased expression levels of cytokines genes IL1Β and MCP1. TNFA expression was decreased by 50 μM, 10 μM of EPA, DHA and with 50 μM EPA + DHA. Two genes involved in the fatty acid metabolism (PTGS2 and ALOX5) were also modulated by the n-3 FAs. 50 μM of DHA and EPA + DHA inhibited PTGS2 expression when the two concentrations of EPA, 50 μM DHA and EPA + DHA inhibited ALOX5 expression. Finally, the effects of n-3 FAs were studied among genes involved in the oxidative stress. 50 μM of each fatty acid increased MGST1 expression. Both concentration of EPA and 50 μM DHA decreased NOS2 expression. CONCLUSION: EPA seems to be more effective than DHA and EPA + DHA in modulating expression levels of selected inflammatory genes. The concentration of 50 μM was globally more effective than 10 μM. BioMed Central 2016-04-05 /pmc/articles/PMC4820929/ /pubmed/27044314 http://dx.doi.org/10.1186/s12944-016-0241-4 Text en © Allam-Ndoul et al. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Allam-Ndoul, Bénédicte
Guénard, Frédéric
Barbier, Olivier
Vohl, Marie-Claude
Effect of n-3 fatty acids on the expression of inflammatory genes in THP-1 macrophages
title Effect of n-3 fatty acids on the expression of inflammatory genes in THP-1 macrophages
title_full Effect of n-3 fatty acids on the expression of inflammatory genes in THP-1 macrophages
title_fullStr Effect of n-3 fatty acids on the expression of inflammatory genes in THP-1 macrophages
title_full_unstemmed Effect of n-3 fatty acids on the expression of inflammatory genes in THP-1 macrophages
title_short Effect of n-3 fatty acids on the expression of inflammatory genes in THP-1 macrophages
title_sort effect of n-3 fatty acids on the expression of inflammatory genes in thp-1 macrophages
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4820929/
https://www.ncbi.nlm.nih.gov/pubmed/27044314
http://dx.doi.org/10.1186/s12944-016-0241-4
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