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Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis
Sevoflurane is generally considered a pro-apoptotic agent in the neonatal brain. However, recent studies have suggested that low levels of sevoflurane anesthesia may be neuroprotective and have a memory enhancing effect. The present study aimed to investigate whether sevoflurane exerts a neuroprotec...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918604/ https://www.ncbi.nlm.nih.gov/pubmed/27222114 http://dx.doi.org/10.3892/mmr.2016.5336 |
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author | ZHOU, ZHI-BIN YANG, XIAO-YU TANG, YING ZHOU, XUE ZHOU, LI-HUA FENG, XIA |
author_facet | ZHOU, ZHI-BIN YANG, XIAO-YU TANG, YING ZHOU, XUE ZHOU, LI-HUA FENG, XIA |
author_sort | ZHOU, ZHI-BIN |
collection | PubMed |
description | Sevoflurane is generally considered a pro-apoptotic agent in the neonatal brain. However, recent studies have suggested that low levels of sevoflurane anesthesia may be neuroprotective and have a memory enhancing effect. The present study aimed to investigate whether sevoflurane exerts a neuroprotective effect at subclinical concentrations, with regard to oxidative state. In the current study, postnatal day 7 (P7) Sprague-Dawley rats were continuously exposed to 0.3, 1.3, or 2.3% sevoflurane for 6 h. ELISA was used to quantify the levels of superoxide dismutase, glutathione peroxidase (GSH-px) and malondialdehyde (MDA) in the plasma and the hippocampus. Terminal deoxynucleotidyl-transferase dUTP nick-end labeling staining was used to observe hippocampal neuronal apoptosis. Altered object exploration tests for recognition memory were employed to investigate long-term behavioral effects at postnatal day 28. The results demonstrated that a single 6 h exposure to a subclinical concentration (1.3%) of sevoflurane at P7 reduces MDA and GPH-px production in rats. Sevoflurane induced hippocampal apoptosis in a dose-dependent manner and altered recognition memory testing indicated no differences among the groups. Although early exposure to a subclinical concentration of sevoflurane reduced oxidative stress, it did not prevent the process of sevoflurane-induced hippocampal apoptosis. These changes did not affect subsequent recognition memory in juvenile rats. |
format | Online Article Text |
id | pubmed-4918604 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-49186042016-07-11 Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis ZHOU, ZHI-BIN YANG, XIAO-YU TANG, YING ZHOU, XUE ZHOU, LI-HUA FENG, XIA Mol Med Rep Articles Sevoflurane is generally considered a pro-apoptotic agent in the neonatal brain. However, recent studies have suggested that low levels of sevoflurane anesthesia may be neuroprotective and have a memory enhancing effect. The present study aimed to investigate whether sevoflurane exerts a neuroprotective effect at subclinical concentrations, with regard to oxidative state. In the current study, postnatal day 7 (P7) Sprague-Dawley rats were continuously exposed to 0.3, 1.3, or 2.3% sevoflurane for 6 h. ELISA was used to quantify the levels of superoxide dismutase, glutathione peroxidase (GSH-px) and malondialdehyde (MDA) in the plasma and the hippocampus. Terminal deoxynucleotidyl-transferase dUTP nick-end labeling staining was used to observe hippocampal neuronal apoptosis. Altered object exploration tests for recognition memory were employed to investigate long-term behavioral effects at postnatal day 28. The results demonstrated that a single 6 h exposure to a subclinical concentration (1.3%) of sevoflurane at P7 reduces MDA and GPH-px production in rats. Sevoflurane induced hippocampal apoptosis in a dose-dependent manner and altered recognition memory testing indicated no differences among the groups. Although early exposure to a subclinical concentration of sevoflurane reduced oxidative stress, it did not prevent the process of sevoflurane-induced hippocampal apoptosis. These changes did not affect subsequent recognition memory in juvenile rats. D.A. Spandidos 2016-07 2016-05-24 /pmc/articles/PMC4918604/ /pubmed/27222114 http://dx.doi.org/10.3892/mmr.2016.5336 Text en Copyright: © Zhou et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles ZHOU, ZHI-BIN YANG, XIAO-YU TANG, YING ZHOU, XUE ZHOU, LI-HUA FENG, XIA Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis |
title | Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis |
title_full | Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis |
title_fullStr | Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis |
title_full_unstemmed | Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis |
title_short | Subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis |
title_sort | subclinical concentrations of sevoflurane reduce oxidative stress but do not prevent hippocampal apoptosis |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4918604/ https://www.ncbi.nlm.nih.gov/pubmed/27222114 http://dx.doi.org/10.3892/mmr.2016.5336 |
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