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Effects of Enteric Environmental Modification by Coffee Components on Neurodegeneration in Rotenone-Treated Mice
Epidemiological studies have shown that coffee consumption decreases the risk of Parkinson’s disease (PD). Caffeic acid (CA) and chlorogenic acid (CGA) are coffee components that have antioxidative properties. Rotenone, a mitochondrial complex I inhibitor, has been used to develop parkinsonian model...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468520/ https://www.ncbi.nlm.nih.gov/pubmed/30866481 http://dx.doi.org/10.3390/cells8030221 |
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author | Miyazaki, Ikuko Isooka, Nami Wada, Kouichi Kikuoka, Ryo Kitamura, Yoshihisa Asanuma, Masato |
author_facet | Miyazaki, Ikuko Isooka, Nami Wada, Kouichi Kikuoka, Ryo Kitamura, Yoshihisa Asanuma, Masato |
author_sort | Miyazaki, Ikuko |
collection | PubMed |
description | Epidemiological studies have shown that coffee consumption decreases the risk of Parkinson’s disease (PD). Caffeic acid (CA) and chlorogenic acid (CGA) are coffee components that have antioxidative properties. Rotenone, a mitochondrial complex I inhibitor, has been used to develop parkinsonian models, because the toxin induces PD-like pathology. Here, we examined the neuroprotective effects of CA and CGA against the rotenone-induced degeneration of central dopaminergic and peripheral enteric neurons. Male C57BL/6J mice were chronically administered rotenone (2.5 mg/kg/day), subcutaneously for four weeks. The animals were orally administered CA or CGA daily for 1 week before rotenone exposure and during the four weeks of rotenone treatment. Administrations of CA or CGA prevented rotenone-induced neurodegeneration of both nigral dopaminergic and intestinal enteric neurons. CA and CGA upregulated the antioxidative molecules, metallothionein (MT)-1,2, in striatal astrocytes of rotenone-injected mice. Primary cultured mesencephalic or enteric cells were pretreated with CA or CGA for 24 h, and then further co-treated with a low dose of rotenone (1–5 nM) for 48 h. The neuroprotective effects and MT upregulation induced by CA and CGA in vivo were reproduced in cultured cells. Our data indicated that intake of coffee components, CA and CGA, enhanced the antioxidative properties of glial cells and prevents rotenone-induced neurodegeneration in both the brain and myenteric plexus. |
format | Online Article Text |
id | pubmed-6468520 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-64685202019-04-23 Effects of Enteric Environmental Modification by Coffee Components on Neurodegeneration in Rotenone-Treated Mice Miyazaki, Ikuko Isooka, Nami Wada, Kouichi Kikuoka, Ryo Kitamura, Yoshihisa Asanuma, Masato Cells Article Epidemiological studies have shown that coffee consumption decreases the risk of Parkinson’s disease (PD). Caffeic acid (CA) and chlorogenic acid (CGA) are coffee components that have antioxidative properties. Rotenone, a mitochondrial complex I inhibitor, has been used to develop parkinsonian models, because the toxin induces PD-like pathology. Here, we examined the neuroprotective effects of CA and CGA against the rotenone-induced degeneration of central dopaminergic and peripheral enteric neurons. Male C57BL/6J mice were chronically administered rotenone (2.5 mg/kg/day), subcutaneously for four weeks. The animals were orally administered CA or CGA daily for 1 week before rotenone exposure and during the four weeks of rotenone treatment. Administrations of CA or CGA prevented rotenone-induced neurodegeneration of both nigral dopaminergic and intestinal enteric neurons. CA and CGA upregulated the antioxidative molecules, metallothionein (MT)-1,2, in striatal astrocytes of rotenone-injected mice. Primary cultured mesencephalic or enteric cells were pretreated with CA or CGA for 24 h, and then further co-treated with a low dose of rotenone (1–5 nM) for 48 h. The neuroprotective effects and MT upregulation induced by CA and CGA in vivo were reproduced in cultured cells. Our data indicated that intake of coffee components, CA and CGA, enhanced the antioxidative properties of glial cells and prevents rotenone-induced neurodegeneration in both the brain and myenteric plexus. MDPI 2019-03-07 /pmc/articles/PMC6468520/ /pubmed/30866481 http://dx.doi.org/10.3390/cells8030221 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Miyazaki, Ikuko Isooka, Nami Wada, Kouichi Kikuoka, Ryo Kitamura, Yoshihisa Asanuma, Masato Effects of Enteric Environmental Modification by Coffee Components on Neurodegeneration in Rotenone-Treated Mice |
title | Effects of Enteric Environmental Modification by Coffee Components on Neurodegeneration in Rotenone-Treated Mice |
title_full | Effects of Enteric Environmental Modification by Coffee Components on Neurodegeneration in Rotenone-Treated Mice |
title_fullStr | Effects of Enteric Environmental Modification by Coffee Components on Neurodegeneration in Rotenone-Treated Mice |
title_full_unstemmed | Effects of Enteric Environmental Modification by Coffee Components on Neurodegeneration in Rotenone-Treated Mice |
title_short | Effects of Enteric Environmental Modification by Coffee Components on Neurodegeneration in Rotenone-Treated Mice |
title_sort | effects of enteric environmental modification by coffee components on neurodegeneration in rotenone-treated mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468520/ https://www.ncbi.nlm.nih.gov/pubmed/30866481 http://dx.doi.org/10.3390/cells8030221 |
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