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Troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis
Alzheimer's disease (AD) is an age-related neurodegenerative disease linked with increased production and/or deposition of amyloid-beta (Aβ) in the brain. The aim of the present study was to investigate the possible neuroprotective effect of troxerutin on an animal model of Alzheimer's dis...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Leibniz Research Centre for Working Environment and Human Factors
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5735350/ https://www.ncbi.nlm.nih.gov/pubmed/29285004 http://dx.doi.org/10.17179/excli2017-526 |
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author | Farajdokht, Fereshteh Amani, Mohammad Mirzaei Bavil, Fariba Alihemmati, Alireza Mohaddes, Gisou Babri, Shirin |
author_facet | Farajdokht, Fereshteh Amani, Mohammad Mirzaei Bavil, Fariba Alihemmati, Alireza Mohaddes, Gisou Babri, Shirin |
author_sort | Farajdokht, Fereshteh |
collection | PubMed |
description | Alzheimer's disease (AD) is an age-related neurodegenerative disease linked with increased production and/or deposition of amyloid-beta (Aβ) in the brain. The aim of the present study was to investigate the possible neuroprotective effect of troxerutin on an animal model of Alzheimer's disease. Alzheimer model was induced by a single dose intracerebroventricular (ICV) injection of Aβ 1-42 (5 nmol/5 µl). Thereafter, troxerutin (300 mg/kg) was gavaged for 14 days. The hippocampal malondialdehyde (MDA) levels and enzymatic activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), and acetylcholinesterase (AChE) were measured using enzyme-linked immunosorbent assay (ELISA) method. In addition, the number of apoptotic cells in the dentate gyrus (DG) was assessed by TUNEL kit. The results showed that ICV microinjection of Aβ 1-42 increased MDA levels, reduced SOD and GPx, and increased AChE activities in the hippocampus. Chronic administration of troxerutin significantly attenuated MDA levels and AChE activity and increased SOD and GPx activities in the hippocampus. Moreover, the number of apoptotic cells was decreased by troxerutin treatment. Taken together, our study demonstrated that troxerutin could increase the resistance of hippocampal neurons against apoptosis, at least in part, by diminishing the activity of AChE and oxidative stress. Therefore, troxerutin may have beneficial effects in the management of Alzheimer's disease. |
format | Online Article Text |
id | pubmed-5735350 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Leibniz Research Centre for Working Environment and Human Factors |
record_format | MEDLINE/PubMed |
spelling | pubmed-57353502017-12-28 Troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis Farajdokht, Fereshteh Amani, Mohammad Mirzaei Bavil, Fariba Alihemmati, Alireza Mohaddes, Gisou Babri, Shirin EXCLI J Original Article Alzheimer's disease (AD) is an age-related neurodegenerative disease linked with increased production and/or deposition of amyloid-beta (Aβ) in the brain. The aim of the present study was to investigate the possible neuroprotective effect of troxerutin on an animal model of Alzheimer's disease. Alzheimer model was induced by a single dose intracerebroventricular (ICV) injection of Aβ 1-42 (5 nmol/5 µl). Thereafter, troxerutin (300 mg/kg) was gavaged for 14 days. The hippocampal malondialdehyde (MDA) levels and enzymatic activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), and acetylcholinesterase (AChE) were measured using enzyme-linked immunosorbent assay (ELISA) method. In addition, the number of apoptotic cells in the dentate gyrus (DG) was assessed by TUNEL kit. The results showed that ICV microinjection of Aβ 1-42 increased MDA levels, reduced SOD and GPx, and increased AChE activities in the hippocampus. Chronic administration of troxerutin significantly attenuated MDA levels and AChE activity and increased SOD and GPx activities in the hippocampus. Moreover, the number of apoptotic cells was decreased by troxerutin treatment. Taken together, our study demonstrated that troxerutin could increase the resistance of hippocampal neurons against apoptosis, at least in part, by diminishing the activity of AChE and oxidative stress. Therefore, troxerutin may have beneficial effects in the management of Alzheimer's disease. Leibniz Research Centre for Working Environment and Human Factors 2017-08-09 /pmc/articles/PMC5735350/ /pubmed/29285004 http://dx.doi.org/10.17179/excli2017-526 Text en Copyright © 2017 Farajdokht et al. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Licence (http://creativecommons.org/licenses/by/4.0/) You are free to copy, distribute and transmit the work, provided the original author and source are credited. |
spellingShingle | Original Article Farajdokht, Fereshteh Amani, Mohammad Mirzaei Bavil, Fariba Alihemmati, Alireza Mohaddes, Gisou Babri, Shirin Troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis |
title | Troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis |
title_full | Troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis |
title_fullStr | Troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis |
title_full_unstemmed | Troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis |
title_short | Troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis |
title_sort | troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5735350/ https://www.ncbi.nlm.nih.gov/pubmed/29285004 http://dx.doi.org/10.17179/excli2017-526 |
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