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  4. Neurological Restorative Effects of (-)-Epicatechin in a Model of Gulf War Illness
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Neurological Restorative Effects of (-)-Epicatechin in a Model of Gulf War Illness

Journal
Journal of Medicinal Food
ISSN
1096-620X
1557-7600
Publisher
Mary Ann Liebert
Date Issued
2024
Author(s)
Ramirez-Sanchez, Israel
Navarrete-Yañez, Viridiana
Espinosa-Raya, Judith
Rubio-Gayosso, Ivan
Palma-Flores, Carlos
Mendoza-Lorenzo, Patricia
Ordoñez-Razo, Rosa
Estrada Mena, Francisco Javier  
Facultad de Ciencias de la Salud - CampCM  
Ceballos, Guillermo
Villarreal, Francisco
Type
text::journal::journal article
DOI
10.1089/jmf.2023.0200
URL
https://scripta.up.edu.mx/handle/20.500.12552/11535
Abstract
Gulf War Illness (GWI) afflicts US military personnel who served in the Persian Gulf War. Suspect causal agents include exposure to pyridostigmine (PB), permethrin (PM) and N,N-diethyl-m-toluamide (DEET). Prominent symptoms include cognitive deficits, such as memory impairment. In aging animal models, we have documented the beneficial effect of the flavanol (-)-epicatechin (Epi) on hippocampus structure and related function. Using a rat model of GWI, we examined the effects of Epi on hippocampus inflammation, oxidative stress, mitochondrial dysfunction, cell death/survival pathways, and memory endpoints. Male Wistar rats underwent 3 weeks of exposure to either vehicles or DEET, PM, PB, and stress. Subgroups of GWI rats were then allocated to receive orally 15 days of either water (vehicle) or 1 mg/kg/day of Epi treatment. Object recognition tasks were performed to assess memory. Hippocampus samples were analyzed. Epi treatment yields significant improvements in short- and long-term memory versus GWI rats. Hippocampus oxidative stress and pro-inflammatory cytokine levels showed significant increases with GWI that were largely normalized with Epi becoming comparable to controls. Significant increases in markers of hippocampus neuroinflammation and cell death were noted with GWI and were also largely reduced with Epi. Neuronal survival signaling pathways were adversely impacted by GWI and were partially or fully restored by Epi. Markers of mitochondrial function were adversely impacted by GWI and were fully restored by Epi. In conclusion, in an animal model of GWI, Epi beneficially impacts recognized markers of hippocampus neuroinflammation, oxidative stress, cell survival, neurotoxicity and mitochondrial function leading to improved memory. ©The authors ©Journal of Medicinal Food ©Mary Ann Liebert.
License
Acceso Restringido
How to cite
Ramirez-Sanchez, I., Navarrete-Yañez, V., Espinosa-Raya, J., Rubio-Gayosso, I., Palma-Flores, C., Mendoza-Lorenzo, P., Ordoñez-Razo, R., Estrada-Mena, J., Ceballos, G., & Villarreal, F. (2024). Neurological Restorative Effects of (-)-Epicatechin in a Model of Gulf War Illness. In Journal of Medicinal Food. Mary Ann Liebert Inc. https://doi.org/10.1089/jmf.2023.0200

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