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Neurological Restorative Effects of (-)-Epicatechin in a Model of Gulf War Illness.
Ramirez-Sanchez, Israel; Navarrete-Yañez, Viridiana; Espinosa-Raya, Judith; Rubio-Gayosso, Ivan; Palma-Flores, Carlos; Mendoza-Lorenzo, Patricia; Ordoñez-Razo, Rosa; Estrada-Mena, Javier; Ceballos, Guillermo; Villarreal, Francisco.
Afiliación
  • Ramirez-Sanchez I; School of Medicine, UCSD, La Jolla, California, USA.
  • Navarrete-Yañez V; Seccion de Estudios de Posgrado e Investigacion, Escuela Superior de Medicina, IPN, Ciudad de Mexico, Mexico.
  • Espinosa-Raya J; Seccion de Estudios de Posgrado e Investigacion, Escuela Superior de Medicina, IPN, Ciudad de Mexico, Mexico.
  • Rubio-Gayosso I; Seccion de Estudios de Posgrado e Investigacion, Escuela Superior de Medicina, IPN, Ciudad de Mexico, Mexico.
  • Palma-Flores C; Seccion de Estudios de Posgrado e Investigacion, Escuela Superior de Medicina, IPN, Ciudad de Mexico, Mexico.
  • Mendoza-Lorenzo P; Seccion de Estudios de Posgrado e Investigacion, Escuela Superior de Medicina, IPN, Ciudad de Mexico, Mexico.
  • Ordoñez-Razo R; Division Academica de Ciencias Basicas, Unidad Chontalpa, Universidad Juarez Autonoma de Tabasco, Villahermosa, Mexico.
  • Estrada-Mena J; Unidad de Investigacion Medica en Genetica Humana, Hosital de Pediatria, Centro Médico Nacional Siglo XXI, Ciudad de Mexico, México.
  • Ceballos G; Escuela de Medicina, Universidad Panamericana, Benito Juarez, México.
  • Villarreal F; Seccion de Estudios de Posgrado e Investigacion, Escuela Superior de Medicina, IPN, Ciudad de Mexico, Mexico.
J Med Food ; 2024 Sep 25.
Article en En | MEDLINE | ID: mdl-39321070
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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: J Med Food Asunto de la revista: CIENCIAS DA NUTRICAO / MEDICINA Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: J Med Food Asunto de la revista: CIENCIAS DA NUTRICAO / MEDICINA Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos