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Life Sci. 2015 Mar 1;124:120-7. doi: 10.1016/j.lfs.2015.01.013. Epub 2015 Jan 28.

Ellagic acid prevents cognitive and hippocampal long-term potentiation deficits and brain inflammation in rat with traumatic brain injury.

Author information

1
Physiology Research Center, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran; Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran.
2
Department of Immunology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran.
3
Physiology Research Center, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran; Department of Physiology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
4
Physiology Research Center, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran; Department of Physiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Golestan Blvd, Ahvaz, Iran. Electronic address: mashhadizadeh.s@ajums.ac.ir.

Abstract

AIMS:

Traumatic brain injury (TBI) remains one of the main clinical problems globally and is a common cause of death among youth. Cognitive defects such as thinking, memory and behavior or mental health disorders are considered as the most frequent effects of severe and moderate TBI. It has been reported that ellagic acid (EA), a natural polyphenol, exhibits protective effects against oxidative damage. This study was performed to examine the EA preventive effects on cognitive impairments, long-term potentiation (LTP) deficits in hippocampus and brain inflammation induced by diffuse TBI in rat.

MAIN METHODS:

Subchronic oral administration of 100 mg/kg EA, 7 consecutive days before induction of trauma (once daily) was used to elucidate the EA effects on passive avoidance memory and hippocampal LTP following TBI. To illustrate the possible mechanisms related to the preventive effects of EA on brain function following TBI, brain content of IL-1β, IL-6 and blood-brain barrier (BBB) permeability were determined.

KEY FINDINGS:

EA pretreatment significantly (P<0.001) prevented TBI-induced memory and hippocampal LTP impairments in rat. Furthermore TBI induced elevation in brain content of IL-1β, IL-6 and BBB permeability were decreased significantly (P<0.001) due to EA pre-treatment.

SIGNIFICANCE:

Our findings suggest that EA can prevent cognitive and LTP deficits and also prevent brain inflammation following TBI.

KEYWORDS:

Dimethyl sulfoxide (PubChem CID: 679); Ellagic acid; Ellagic acid (PubChem CID: 5281855); Evans blue (PubChem CID: 6321418); IL-1β; IL-6; Long term potentiation; Potassium chloride (PubChem CID: 4873); Potassium phosphate (PubChem CID: 516951); Sodium chloride (PubChem CID: 5234); Sodium phosphate (PubChem CID: 23672064); Traumatic brain injury; Tris base (PubChem CID: 6503); Triton X-100 (PubChem CID: 5590)

PMID:
25637685
DOI:
10.1016/j.lfs.2015.01.013
[Indexed for MEDLINE]

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