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α-Tocopherol Ameliorates Redox Equilibrium and Reduces Inflammatory Response Caused by Chronic Variable Stress

Chronic exposure to stress factors contributes to the development of depression by generating excess of reactive oxygen species which leads to oxidative stress and inflammatory processes. The aim of the study was to assess the potential protective properties of α-tocopherol supplementation on the ra...

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Autores principales: Herbet, Mariola, Izdebska, Magdalena, Piątkowska-Chmiel, Iwona, Gawrońska-Grzywacz, Monika, Natorska-Chomicka, Dorota, Pawłowski, Kamil, Sysa, Marcin, Ślaska, Brygida, Dudka, Jarosław
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6250045/
https://www.ncbi.nlm.nih.gov/pubmed/30533439
http://dx.doi.org/10.1155/2018/7210783
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author Herbet, Mariola
Izdebska, Magdalena
Piątkowska-Chmiel, Iwona
Gawrońska-Grzywacz, Monika
Natorska-Chomicka, Dorota
Pawłowski, Kamil
Sysa, Marcin
Ślaska, Brygida
Dudka, Jarosław
author_facet Herbet, Mariola
Izdebska, Magdalena
Piątkowska-Chmiel, Iwona
Gawrońska-Grzywacz, Monika
Natorska-Chomicka, Dorota
Pawłowski, Kamil
Sysa, Marcin
Ślaska, Brygida
Dudka, Jarosław
author_sort Herbet, Mariola
collection PubMed
description Chronic exposure to stress factors contributes to the development of depression by generating excess of reactive oxygen species which leads to oxidative stress and inflammatory processes. The aim of the study was to assess the potential protective properties of α-tocopherol supplementation on the rats exposed to chronic variable stress (CVS). Male Wistar rats (50-55 days old, weighing 200-250 g) were divided into three groups (n=10): control, stressed, and stressed and receiving (+)-α-tocopherol solution in a dose of 100 mg/kg/day. Rats in the stressed groups were exposed to CVS for 40 days. Markers of redox disorders (glutathione reduced and oxidized levels, GSH/GSSG ratio, glutathione peroxidase, glutathione reductase activities, total antioxidant status, and lipid peroxidation) and inflammatory response (IL-1β, IL6, and TNF-α) were determined in the blood. Additionally, molecular biomarkers of depression (expression of Fkbp5 and Tph2) were studied in hippocampus. The biochemical analysis was inconclusive about the presence of oxidative stress in the blood of rats exposed to CVS. However, changes in all parameters suggest presence of redox equilibrium disorders. Similarly, activation of inflammatory processes was observed as a result of CVS. Molecular effects of environmental stress in hippocampus were also observed. Generally, α-tocopherol ameliorated redox equilibrium disorders, tempered inflammatory response, and protected from changes in determined molecular markers of depression.
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spelling pubmed-62500452018-12-09 α-Tocopherol Ameliorates Redox Equilibrium and Reduces Inflammatory Response Caused by Chronic Variable Stress Herbet, Mariola Izdebska, Magdalena Piątkowska-Chmiel, Iwona Gawrońska-Grzywacz, Monika Natorska-Chomicka, Dorota Pawłowski, Kamil Sysa, Marcin Ślaska, Brygida Dudka, Jarosław Biomed Res Int Research Article Chronic exposure to stress factors contributes to the development of depression by generating excess of reactive oxygen species which leads to oxidative stress and inflammatory processes. The aim of the study was to assess the potential protective properties of α-tocopherol supplementation on the rats exposed to chronic variable stress (CVS). Male Wistar rats (50-55 days old, weighing 200-250 g) were divided into three groups (n=10): control, stressed, and stressed and receiving (+)-α-tocopherol solution in a dose of 100 mg/kg/day. Rats in the stressed groups were exposed to CVS for 40 days. Markers of redox disorders (glutathione reduced and oxidized levels, GSH/GSSG ratio, glutathione peroxidase, glutathione reductase activities, total antioxidant status, and lipid peroxidation) and inflammatory response (IL-1β, IL6, and TNF-α) were determined in the blood. Additionally, molecular biomarkers of depression (expression of Fkbp5 and Tph2) were studied in hippocampus. The biochemical analysis was inconclusive about the presence of oxidative stress in the blood of rats exposed to CVS. However, changes in all parameters suggest presence of redox equilibrium disorders. Similarly, activation of inflammatory processes was observed as a result of CVS. Molecular effects of environmental stress in hippocampus were also observed. Generally, α-tocopherol ameliorated redox equilibrium disorders, tempered inflammatory response, and protected from changes in determined molecular markers of depression. Hindawi 2018-11-08 /pmc/articles/PMC6250045/ /pubmed/30533439 http://dx.doi.org/10.1155/2018/7210783 Text en Copyright © 2018 Mariola Herbet et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Herbet, Mariola
Izdebska, Magdalena
Piątkowska-Chmiel, Iwona
Gawrońska-Grzywacz, Monika
Natorska-Chomicka, Dorota
Pawłowski, Kamil
Sysa, Marcin
Ślaska, Brygida
Dudka, Jarosław
α-Tocopherol Ameliorates Redox Equilibrium and Reduces Inflammatory Response Caused by Chronic Variable Stress
title α-Tocopherol Ameliorates Redox Equilibrium and Reduces Inflammatory Response Caused by Chronic Variable Stress
title_full α-Tocopherol Ameliorates Redox Equilibrium and Reduces Inflammatory Response Caused by Chronic Variable Stress
title_fullStr α-Tocopherol Ameliorates Redox Equilibrium and Reduces Inflammatory Response Caused by Chronic Variable Stress
title_full_unstemmed α-Tocopherol Ameliorates Redox Equilibrium and Reduces Inflammatory Response Caused by Chronic Variable Stress
title_short α-Tocopherol Ameliorates Redox Equilibrium and Reduces Inflammatory Response Caused by Chronic Variable Stress
title_sort α-tocopherol ameliorates redox equilibrium and reduces inflammatory response caused by chronic variable stress
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6250045/
https://www.ncbi.nlm.nih.gov/pubmed/30533439
http://dx.doi.org/10.1155/2018/7210783
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