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Astaxanthin ameliorates prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring
BACKGROUND: Prenatal maternal lipopolysaccharide (LPS) exposure leads to behavioral deficits such as depression, anxiety, and schizophrenia in the adult lives. LPS-exposure resulted in the production of cytokines and oxidative damage. On the contrary, astaxanthin is a carotenoid compound, showed neu...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4746928/ https://www.ncbi.nlm.nih.gov/pubmed/26856812 http://dx.doi.org/10.1186/s12868-016-0245-z |
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author | Al-Amin, Md. Mamun Sultana, Rabeya Sultana, Sharmin Rahman, Md. Mahbubur Reza, Hasan Mahmud |
author_facet | Al-Amin, Md. Mamun Sultana, Rabeya Sultana, Sharmin Rahman, Md. Mahbubur Reza, Hasan Mahmud |
author_sort | Al-Amin, Md. Mamun |
collection | PubMed |
description | BACKGROUND: Prenatal maternal lipopolysaccharide (LPS) exposure leads to behavioral deficits such as depression, anxiety, and schizophrenia in the adult lives. LPS-exposure resulted in the production of cytokines and oxidative damage. On the contrary, astaxanthin is a carotenoid compound, showed neuroprotective properties via its antioxidant capacity. This study examines the effect of astaxanthin on the prenatal maternal LPS-induced postnatal behavioral deficit in mice. RESULTS: We found that prenatal LPS-exposed mice showed extensive immobile phase in the tail suspension test, higher frequent head dipping in the hole-board test and greater hypolocomotion in the open field test. All these values were statistically significant (p < 0.05). In addition, a marked elevation of the level of lipid peroxidation, advanced protein oxidation product, nitric oxide, while a pronounced depletion of antioxidant enzymes (superoxide dismutase, catalase and glutathione) were observed in the adult offspring mice that were prenatally exposed to LPS. To the contrary, 6-weeks long treatment with astaxanthin significantly improved all behavioral deficits (p < 0.05) and diminished prenatal LPS-induced oxidative stress markers in the brain and liver. CONCLUSIONS: Taken together, these results suggest that prenatal maternal LPS-exposure leads to behavioral deficits in the adults, while astaxanthin ameliorates the behavioral deficits presumably via its antioxidant property. |
format | Online Article Text |
id | pubmed-4746928 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-47469282016-02-10 Astaxanthin ameliorates prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring Al-Amin, Md. Mamun Sultana, Rabeya Sultana, Sharmin Rahman, Md. Mahbubur Reza, Hasan Mahmud BMC Neurosci Research Article BACKGROUND: Prenatal maternal lipopolysaccharide (LPS) exposure leads to behavioral deficits such as depression, anxiety, and schizophrenia in the adult lives. LPS-exposure resulted in the production of cytokines and oxidative damage. On the contrary, astaxanthin is a carotenoid compound, showed neuroprotective properties via its antioxidant capacity. This study examines the effect of astaxanthin on the prenatal maternal LPS-induced postnatal behavioral deficit in mice. RESULTS: We found that prenatal LPS-exposed mice showed extensive immobile phase in the tail suspension test, higher frequent head dipping in the hole-board test and greater hypolocomotion in the open field test. All these values were statistically significant (p < 0.05). In addition, a marked elevation of the level of lipid peroxidation, advanced protein oxidation product, nitric oxide, while a pronounced depletion of antioxidant enzymes (superoxide dismutase, catalase and glutathione) were observed in the adult offspring mice that were prenatally exposed to LPS. To the contrary, 6-weeks long treatment with astaxanthin significantly improved all behavioral deficits (p < 0.05) and diminished prenatal LPS-induced oxidative stress markers in the brain and liver. CONCLUSIONS: Taken together, these results suggest that prenatal maternal LPS-exposure leads to behavioral deficits in the adults, while astaxanthin ameliorates the behavioral deficits presumably via its antioxidant property. BioMed Central 2016-02-08 /pmc/articles/PMC4746928/ /pubmed/26856812 http://dx.doi.org/10.1186/s12868-016-0245-z Text en © Al-Amin et al. 2016 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 Al-Amin, Md. Mamun Sultana, Rabeya Sultana, Sharmin Rahman, Md. Mahbubur Reza, Hasan Mahmud Astaxanthin ameliorates prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring |
title | Astaxanthin ameliorates prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring |
title_full | Astaxanthin ameliorates prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring |
title_fullStr | Astaxanthin ameliorates prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring |
title_full_unstemmed | Astaxanthin ameliorates prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring |
title_short | Astaxanthin ameliorates prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring |
title_sort | astaxanthin ameliorates prenatal lps-exposed behavioral deficits and oxidative stress in adult offspring |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4746928/ https://www.ncbi.nlm.nih.gov/pubmed/26856812 http://dx.doi.org/10.1186/s12868-016-0245-z |
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