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BMC Neurosci. 2016 Feb 8;17:11. doi: 10.1186/s12868-016-0245-z.

Astaxanthin ameliorates prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring.

Author information

1
Department of Pharmaceutical Sciences, North South University, Plot 15, Block B, Bashundhara, Dhaka, 1229, Bangladesh. mamun.al-amin@northsouth.edu.
2
The Queensland Brain Institute, The University of Queensland, St. Lucia, Brisbane, QLD, 4072, Australia. mamun.al-amin@northsouth.edu.
3
Department of Pharmaceutical Sciences, North South University, Plot 15, Block B, Bashundhara, Dhaka, 1229, Bangladesh. rbysltntama@yahoo.com.
4
Department of Pharmaceutical Sciences, North South University, Plot 15, Block B, Bashundhara, Dhaka, 1229, Bangladesh. sharmin.sultana@northsouth.edu.
5
Department of Pharmaceutical Sciences, North South University, Plot 15, Block B, Bashundhara, Dhaka, 1229, Bangladesh. rahman.mahbubur@northsouth.edu.
6
Department of Pharmaceutical Sciences, North South University, Plot 15, Block B, Bashundhara, Dhaka, 1229, Bangladesh. hasan.reza@northsouth.edu.

Abstract

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.

PMID:
26856812
PMCID:
PMC4746928
DOI:
10.1186/s12868-016-0245-z
[Indexed for MEDLINE]
Free PMC Article

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