Gallic acid improves recognition memory and decreases oxidative-inflammatory damage in the rat hippocampus with metabolic syndrome
Por:
Diaz A., Muñoz-Arenas G., Caporal-Hernandez K., Vázquez-Roque R., Lopez-Lopez G., Kozina A., Espinosa B., Flores G., Treviño S., Guevara J.
Publicada:
1 feb 2021
Ahead of Print:
1 ene 2020
Categoría:
Cellular and molecular neuroscience
Resumen:
Metabolic syndrome (MS) results from excessive consumption of high-calorie foods and sedentary lifestyles. Clinically, insulin resistance, abdominal obesity, hyperglycemia, dyslipidemia, and hypertension are observed. MS has been considered a risk factor in the development of dementia. In the brain, a metabolically impaired environment generates oxidative stress and excessive production of pro-inflammatory cytokines that deteriorate the morphology and neuronal function in the hippocampus, leading to cognitive impairment. Therapeutic alternatives suggest that phenolic compounds can be part of the treatment for neuropathies and metabolic diseases. In recent years, the use of Gallic Acid (GA) has demonstrated antioxidant and anti-inflammatory effects that contribute to neuroprotection and memory improvement in animal models. However, the effect of GA on hippocampal neurodegeneration and memory impairment under MS conditions is still unclear. In this work, we administered GA (20 mg/kg) for 60 days to rats with MS. The results show that GA treatment improved zoometric and biochemical parameters, as well as the recognition memory, in animals with MS. Additionally, GA administration increased hippocampal dendritic spines and decreased oxidative stress and inflammation. Our results show that GA treatment improves metabolism: reducing the oxidative and inflammatory environment that facilitates the recovery of the neuronal morphology in the hippocampus of rats with MS. Consequently, the recognition of objects by these animals, suggesting that GA could be used therapeutically in metabolic disorders that cause dementia. © 2020 Wiley Periodicals LLC
Filiaciones:
Diaz A.:
Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Mexico
Muñoz-Arenas G.:
Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Mexico
Caporal-Hernandez K.:
Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Mexico
Vázquez-Roque R.:
Laboratorio de Neuropsiquiatria, Instituto de Fisiologia, Benemerita Universidad Autonoma de Puebla, Puebla, Mexico
Lopez-Lopez G.:
Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Mexico
Kozina A.:
Instituto de Química, Universidad Nacional Autónoma de México, Ciudad de México, Mexico
Espinosa B.:
Departamento de Bioquimica, Instituto Nacional de Enfermedades Respiratorias, ICV, Ciudad de Mexico, Mexico
Flores G.:
Laboratorio de Neuropsiquiatria, Instituto de Fisiologia, Benemerita Universidad Autonoma de Puebla, Puebla, Mexico
Treviño S.:
Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Mexico
Guevara J.:
Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico
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