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Dietary phenethylisothiocyanate attenuates bowel inflammation in mice
BACKGROUND: Phenethylisothiocyanate (PEITC) is produced by Brassica food plants. PEO is a PEITC Essential Oil containing >95% natural PEITC. PEITC is known to produce various health benefits but its effect in alleviation of ulcerative colitis signs is unknown. RESULTS: In two efficacy studies (ac...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2881005/ https://www.ncbi.nlm.nih.gov/pubmed/20423518 http://dx.doi.org/10.1186/1472-6769-10-4 |
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author | Dey, Moul Kuhn, Peter Ribnicky, David Premkumar, VummidiGiridhar Reuhl, Kenneth Raskin, Ilya |
author_facet | Dey, Moul Kuhn, Peter Ribnicky, David Premkumar, VummidiGiridhar Reuhl, Kenneth Raskin, Ilya |
author_sort | Dey, Moul |
collection | PubMed |
description | BACKGROUND: Phenethylisothiocyanate (PEITC) is produced by Brassica food plants. PEO is a PEITC Essential Oil containing >95% natural PEITC. PEITC is known to produce various health benefits but its effect in alleviation of ulcerative colitis signs is unknown. RESULTS: In two efficacy studies (acute and chronic) oral administration of PEO was effective at remitting acute and chronic signs of ulcerative colitis (UC) in mice. Disease activity, histology and biochemical characteristics were measured in the treated animals and were compared with appropriate controls. PEO treatment significantly improved body weights and stool consistency as well as decreased intestinal bleeding. PEO treatment also reduced mucosal inflammation, depletion of goblet cells and infiltration of inflammatory cells. Attenuation of proinflammatory interleukin1β production was observed in the colons of PEO-treated animals. Expression analyses were also carried out for immune function related genes, transcription factors and cytokines in lipopolysaccharide-activated mouse macrophage cells. PEO likely affects an intricate network of immune signaling genes including a novel concentration dependent reduction of total cellular Signal Transducer and Activator of Transcription 1 (STAT1) as well as nuclear phosphorylated-STAT1 (activated form of STAT1). A PEO-concentration dependent decrease of mRNA of C-X-C motif ligand 10 (a STAT1 responsive chemokine) and Interleukin 6 were also observed. CONCLUSIONS: PEO might be a promising candidate to develop as a treatment for ulcerative colitis patients. The disease attenuation by PEO is likely associated with suppression of activation of STAT1 transcription and inhibition of pro-inflammatory cytokines. |
format | Text |
id | pubmed-2881005 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-28810052010-06-05 Dietary phenethylisothiocyanate attenuates bowel inflammation in mice Dey, Moul Kuhn, Peter Ribnicky, David Premkumar, VummidiGiridhar Reuhl, Kenneth Raskin, Ilya BMC Chem Biol Research article BACKGROUND: Phenethylisothiocyanate (PEITC) is produced by Brassica food plants. PEO is a PEITC Essential Oil containing >95% natural PEITC. PEITC is known to produce various health benefits but its effect in alleviation of ulcerative colitis signs is unknown. RESULTS: In two efficacy studies (acute and chronic) oral administration of PEO was effective at remitting acute and chronic signs of ulcerative colitis (UC) in mice. Disease activity, histology and biochemical characteristics were measured in the treated animals and were compared with appropriate controls. PEO treatment significantly improved body weights and stool consistency as well as decreased intestinal bleeding. PEO treatment also reduced mucosal inflammation, depletion of goblet cells and infiltration of inflammatory cells. Attenuation of proinflammatory interleukin1β production was observed in the colons of PEO-treated animals. Expression analyses were also carried out for immune function related genes, transcription factors and cytokines in lipopolysaccharide-activated mouse macrophage cells. PEO likely affects an intricate network of immune signaling genes including a novel concentration dependent reduction of total cellular Signal Transducer and Activator of Transcription 1 (STAT1) as well as nuclear phosphorylated-STAT1 (activated form of STAT1). A PEO-concentration dependent decrease of mRNA of C-X-C motif ligand 10 (a STAT1 responsive chemokine) and Interleukin 6 were also observed. CONCLUSIONS: PEO might be a promising candidate to develop as a treatment for ulcerative colitis patients. The disease attenuation by PEO is likely associated with suppression of activation of STAT1 transcription and inhibition of pro-inflammatory cytokines. BioMed Central 2010-04-27 /pmc/articles/PMC2881005/ /pubmed/20423518 http://dx.doi.org/10.1186/1472-6769-10-4 Text en Copyright ©2010 Dey et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research article Dey, Moul Kuhn, Peter Ribnicky, David Premkumar, VummidiGiridhar Reuhl, Kenneth Raskin, Ilya Dietary phenethylisothiocyanate attenuates bowel inflammation in mice |
title | Dietary phenethylisothiocyanate attenuates bowel inflammation in mice |
title_full | Dietary phenethylisothiocyanate attenuates bowel inflammation in mice |
title_fullStr | Dietary phenethylisothiocyanate attenuates bowel inflammation in mice |
title_full_unstemmed | Dietary phenethylisothiocyanate attenuates bowel inflammation in mice |
title_short | Dietary phenethylisothiocyanate attenuates bowel inflammation in mice |
title_sort | dietary phenethylisothiocyanate attenuates bowel inflammation in mice |
topic | Research article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2881005/ https://www.ncbi.nlm.nih.gov/pubmed/20423518 http://dx.doi.org/10.1186/1472-6769-10-4 |
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