Protection of Mice from Controlled Cortical Impact Injury by Food Additive Glyceryl Tribenzoate

Despite intense investigations, no effective therapy is available to halt the pathogenesis of traumatic brain injury (TBI), a major health concern, which sometimes leads to long-term neurological disability, especially in war veterans and young adults. This study highlights the use of glyceryl tribe...

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Bibliographic Details
Published in:International journal of molecular sciences 2023-01, Vol.24 (3), p.2083
Main Authors: Rangasamy, Suresh B, Poddar, Jit, Pahan, Kalipada
Format: Article
Language:English
Subjects:
Animal cognition
Animals
Astrocytes
Brain - pathology
Brain Injuries, Traumatic - drug therapy
Brain Injuries, Traumatic - pathology
Disease
Disease control
Disease Models, Animal
Food additives
Food Additives - pharmacology
glial activation
Glutamate receptors
Glutamic acid receptors (ionotropic)
glyceryl tribenzoate
Hippocampus
Inflammation
lesion cavity
memory and learning
Mice
Mice, Inbred C57BL
Microglia
Military personnel
Neurological complications
Neuroprotection
Nitric oxide
Nitric-oxide synthase
Oral administration
Pathogenesis
Postsynaptic density proteins
Proteins
Spatial discrimination learning
Spatial Learning
Spatial memory
TBI
Traumatic brain injury
Young adults
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Summary:Despite intense investigations, no effective therapy is available to halt the pathogenesis of traumatic brain injury (TBI), a major health concern, which sometimes leads to long-term neurological disability, especially in war veterans and young adults. This study highlights the use of glyceryl tribenzoate (GTB), a flavoring ingredient, in ameliorating the disease process of controlled cortical impact (CCI)-induced TBI in mice. Oral administration of GTB decreased the activation of microglia and astrocytes to inhibit the expression of inducible nitric oxide synthase (iNOS) in hippocampus and cortex of TBI mice. Accordingly, GTB treatment protected and/or restored synaptic maturation in the hippocampus of TBI mice as revealed by the status of PSD-95, NR-2A and GluR1. Furthermore, oral GTB also reduced the size of lesion cavity in the brain of TBI mice. Finally, GTB treatment improved locomotor functions and protected spatial learning and memory in TBI mice. These results outline a novel neuroprotective property of GTB which may be beneficial in treatment of TBI.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms24032083