Cargando…
The ethanol extract of Aquilariae Lignum ameliorates hippocampal oxidative stress in a repeated restraint stress mouse model
BACKGROUND: Chronic stress contributes to the development of brain disorders, such as neurodegenerative and psychiatric diseases. Oxidative damage is well known as a causative factor for pathogenic process in brain tissues. The aim of this study is to evaluate the neuroprotective effect of a 30% eth...
Autores principales: | , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5553856/ https://www.ncbi.nlm.nih.gov/pubmed/28797292 http://dx.doi.org/10.1186/s12906-017-1902-1 |
_version_ | 1783256691397099520 |
---|---|
author | Lee, Hyun-Yong Lee, Jin-Seok Kim, Hyeong-Geug Kim, Won-Yong Lee, Seung-Bae Choi, Yung-Hyun Son, Chang-Gue |
author_facet | Lee, Hyun-Yong Lee, Jin-Seok Kim, Hyeong-Geug Kim, Won-Yong Lee, Seung-Bae Choi, Yung-Hyun Son, Chang-Gue |
author_sort | Lee, Hyun-Yong |
collection | PubMed |
description | BACKGROUND: Chronic stress contributes to the development of brain disorders, such as neurodegenerative and psychiatric diseases. Oxidative damage is well known as a causative factor for pathogenic process in brain tissues. The aim of this study is to evaluate the neuroprotective effect of a 30% ethanol extract of Aquilariae Lignum (ALE) in repeated stress-induced hippocampal oxidative injury. METHODS: Fifty BALB/c male mice (12 weeks old) were randomly divided into five groups (n = 10). For 11 consecutive days, each group was orally administered with distilled water, ALE (20 or 80 mg/kg) or N-acetylcysteine (NAC; 100 mg/kg), and then all mice (except unstressed group) were subjected to restraint stress for 6 h. On the final day, brain tissues and sera were isolated, and stress hormones and hippocampal oxidative alterations were examined. We also treated lipopolysaccharide (LPS, 1 μg/mL)-stimulated BV2 microglial cells with ALE (1 and 5 μg/mL) or NAC (10 μM) to investigate the pharmacological mechanism. RESULTS: Restraint stress considerably increased the serum levels of corticosterone and adrenaline and the hippocampal levels of reactive oxygen species (ROS), nitric oxide (NO), and malondialdehyde (MDA). ALE administration significantly attenuated the above abnormalities. ALE also significantly normalized the stress-induced activation of astrocytes and microglial cells in the hippocampus as well as the elevation of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). The in vitro assay outcome supplemented ALE could dramatically block NF-κB activation in microglia. The anti-oxidative stress effects of ALE were supported by the results of antioxidant components, 4-hydroxynonenal (4-HNE), NADPH oxidase 2 (NOX2), inducible nitric oxide synthase (iNOS) and NFE2L2 (Nrf2) in the hippocampal tissues. CONCLUSIONS: We firstly demonstrated the neuroprotective potentials of A. Lignum against hippocampal oxidative injury in repeated restraint stress. The corresponding mechanisms might involve modulations in the release of ROS, pro-inflammatory cytokines and stress hormones. |
format | Online Article Text |
id | pubmed-5553856 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-55538562017-08-15 The ethanol extract of Aquilariae Lignum ameliorates hippocampal oxidative stress in a repeated restraint stress mouse model Lee, Hyun-Yong Lee, Jin-Seok Kim, Hyeong-Geug Kim, Won-Yong Lee, Seung-Bae Choi, Yung-Hyun Son, Chang-Gue BMC Complement Altern Med Research Article BACKGROUND: Chronic stress contributes to the development of brain disorders, such as neurodegenerative and psychiatric diseases. Oxidative damage is well known as a causative factor for pathogenic process in brain tissues. The aim of this study is to evaluate the neuroprotective effect of a 30% ethanol extract of Aquilariae Lignum (ALE) in repeated stress-induced hippocampal oxidative injury. METHODS: Fifty BALB/c male mice (12 weeks old) were randomly divided into five groups (n = 10). For 11 consecutive days, each group was orally administered with distilled water, ALE (20 or 80 mg/kg) or N-acetylcysteine (NAC; 100 mg/kg), and then all mice (except unstressed group) were subjected to restraint stress for 6 h. On the final day, brain tissues and sera were isolated, and stress hormones and hippocampal oxidative alterations were examined. We also treated lipopolysaccharide (LPS, 1 μg/mL)-stimulated BV2 microglial cells with ALE (1 and 5 μg/mL) or NAC (10 μM) to investigate the pharmacological mechanism. RESULTS: Restraint stress considerably increased the serum levels of corticosterone and adrenaline and the hippocampal levels of reactive oxygen species (ROS), nitric oxide (NO), and malondialdehyde (MDA). ALE administration significantly attenuated the above abnormalities. ALE also significantly normalized the stress-induced activation of astrocytes and microglial cells in the hippocampus as well as the elevation of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). The in vitro assay outcome supplemented ALE could dramatically block NF-κB activation in microglia. The anti-oxidative stress effects of ALE were supported by the results of antioxidant components, 4-hydroxynonenal (4-HNE), NADPH oxidase 2 (NOX2), inducible nitric oxide synthase (iNOS) and NFE2L2 (Nrf2) in the hippocampal tissues. CONCLUSIONS: We firstly demonstrated the neuroprotective potentials of A. Lignum against hippocampal oxidative injury in repeated restraint stress. The corresponding mechanisms might involve modulations in the release of ROS, pro-inflammatory cytokines and stress hormones. BioMed Central 2017-08-10 /pmc/articles/PMC5553856/ /pubmed/28797292 http://dx.doi.org/10.1186/s12906-017-1902-1 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Lee, Hyun-Yong Lee, Jin-Seok Kim, Hyeong-Geug Kim, Won-Yong Lee, Seung-Bae Choi, Yung-Hyun Son, Chang-Gue The ethanol extract of Aquilariae Lignum ameliorates hippocampal oxidative stress in a repeated restraint stress mouse model |
title | The ethanol extract of Aquilariae Lignum ameliorates hippocampal oxidative stress in a repeated restraint stress mouse model |
title_full | The ethanol extract of Aquilariae Lignum ameliorates hippocampal oxidative stress in a repeated restraint stress mouse model |
title_fullStr | The ethanol extract of Aquilariae Lignum ameliorates hippocampal oxidative stress in a repeated restraint stress mouse model |
title_full_unstemmed | The ethanol extract of Aquilariae Lignum ameliorates hippocampal oxidative stress in a repeated restraint stress mouse model |
title_short | The ethanol extract of Aquilariae Lignum ameliorates hippocampal oxidative stress in a repeated restraint stress mouse model |
title_sort | ethanol extract of aquilariae lignum ameliorates hippocampal oxidative stress in a repeated restraint stress mouse model |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5553856/ https://www.ncbi.nlm.nih.gov/pubmed/28797292 http://dx.doi.org/10.1186/s12906-017-1902-1 |
work_keys_str_mv | AT leehyunyong theethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT leejinseok theethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT kimhyeonggeug theethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT kimwonyong theethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT leeseungbae theethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT choiyunghyun theethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT sonchanggue theethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT leehyunyong ethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT leejinseok ethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT kimhyeonggeug ethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT kimwonyong ethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT leeseungbae ethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT choiyunghyun ethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel AT sonchanggue ethanolextractofaquilariaelignumameliorateshippocampaloxidativestressinarepeatedrestraintstressmousemodel |