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Rhamnetin attenuates cognitive deficit and inhibits hippocampal inflammatory response and oxidative stress in rats with traumatic brain injury
Activation of the immune system in the central nervous system and oxidative stress play important roles in traumatic brain injury (TBI)-induced cognitive impairment. Rhamnetin possesses anti-inflammatory and anti-oxidative properties. This study aimed to detect the possible effects of rhamnetin on c...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Polish Society of Experimental and Clinical Immunology
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4472538/ https://www.ncbi.nlm.nih.gov/pubmed/26155182 http://dx.doi.org/10.5114/ceji.2015.50831 |
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author | Zhang, Wei Li, Ben Guo, Yan Bai, Yunan Wang, Tongxin Fu, Kun Sun, Gaoling |
author_facet | Zhang, Wei Li, Ben Guo, Yan Bai, Yunan Wang, Tongxin Fu, Kun Sun, Gaoling |
author_sort | Zhang, Wei |
collection | PubMed |
description | Activation of the immune system in the central nervous system and oxidative stress play important roles in traumatic brain injury (TBI)-induced cognitive impairment. Rhamnetin possesses anti-inflammatory and anti-oxidative properties. This study aimed to detect the possible effects of rhamnetin on cognitive deficit, hippocampal inflammatory factors, and oxidative stress in rats with TBI. In this study, we established the traumatic brain injury model in rats. Rats respectively received vehicle saline or rhamnetin for 21 days. Cognitive functions were evaluated by assessing the acquisition of spatial learning and memory retention in Morris Water Maze test from day 15 to 19 post TBI. Levels of interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor a (TNF-a), IL-10, and nuclear factor κB (NF-κB) in hippocampal homogenate were measured using ELISA. Oxidative stress was analysed by investigating the activities of MDA, H2O2, SOD, and GSH-Px. We found that rhamnetin significantly improved cognitive impairment in rats with TBI, and inhibited the inflammatory response and oxidative stress in the hippocampus. The results suggested that rhamnetin could enhance the recovery of cognitive deficits induced by TBI, and that its mechanism might be associated with the inhibition of inflammation and oxidative stress in the hippocampus. |
format | Online Article Text |
id | pubmed-4472538 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Polish Society of Experimental and Clinical Immunology |
record_format | MEDLINE/PubMed |
spelling | pubmed-44725382015-07-07 Rhamnetin attenuates cognitive deficit and inhibits hippocampal inflammatory response and oxidative stress in rats with traumatic brain injury Zhang, Wei Li, Ben Guo, Yan Bai, Yunan Wang, Tongxin Fu, Kun Sun, Gaoling Cent Eur J Immunol Original Article Activation of the immune system in the central nervous system and oxidative stress play important roles in traumatic brain injury (TBI)-induced cognitive impairment. Rhamnetin possesses anti-inflammatory and anti-oxidative properties. This study aimed to detect the possible effects of rhamnetin on cognitive deficit, hippocampal inflammatory factors, and oxidative stress in rats with TBI. In this study, we established the traumatic brain injury model in rats. Rats respectively received vehicle saline or rhamnetin for 21 days. Cognitive functions were evaluated by assessing the acquisition of spatial learning and memory retention in Morris Water Maze test from day 15 to 19 post TBI. Levels of interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor a (TNF-a), IL-10, and nuclear factor κB (NF-κB) in hippocampal homogenate were measured using ELISA. Oxidative stress was analysed by investigating the activities of MDA, H2O2, SOD, and GSH-Px. We found that rhamnetin significantly improved cognitive impairment in rats with TBI, and inhibited the inflammatory response and oxidative stress in the hippocampus. The results suggested that rhamnetin could enhance the recovery of cognitive deficits induced by TBI, and that its mechanism might be associated with the inhibition of inflammation and oxidative stress in the hippocampus. Polish Society of Experimental and Clinical Immunology 2015-04-22 2015 /pmc/articles/PMC4472538/ /pubmed/26155182 http://dx.doi.org/10.5114/ceji.2015.50831 Text en Copyright © Central European Journal of Immunology 2015 http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Zhang, Wei Li, Ben Guo, Yan Bai, Yunan Wang, Tongxin Fu, Kun Sun, Gaoling Rhamnetin attenuates cognitive deficit and inhibits hippocampal inflammatory response and oxidative stress in rats with traumatic brain injury |
title | Rhamnetin attenuates cognitive deficit and inhibits hippocampal inflammatory response and oxidative stress in rats with traumatic brain injury |
title_full | Rhamnetin attenuates cognitive deficit and inhibits hippocampal inflammatory response and oxidative stress in rats with traumatic brain injury |
title_fullStr | Rhamnetin attenuates cognitive deficit and inhibits hippocampal inflammatory response and oxidative stress in rats with traumatic brain injury |
title_full_unstemmed | Rhamnetin attenuates cognitive deficit and inhibits hippocampal inflammatory response and oxidative stress in rats with traumatic brain injury |
title_short | Rhamnetin attenuates cognitive deficit and inhibits hippocampal inflammatory response and oxidative stress in rats with traumatic brain injury |
title_sort | rhamnetin attenuates cognitive deficit and inhibits hippocampal inflammatory response and oxidative stress in rats with traumatic brain injury |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4472538/ https://www.ncbi.nlm.nih.gov/pubmed/26155182 http://dx.doi.org/10.5114/ceji.2015.50831 |
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