Epicatechin Reduces Spatial Memory Deficit Caused by Amyloid-25-35 Toxicity Modifying the Heat Shock Proteins in the CA1 Region in the Hippocampus of Rats
Por:
Diaz, Alfonso, Trevino, Samuel, Pulido-Fernandez, Guadalupe, Martinez-Munoz, Estefania, Cervantes, Nallely, Espinosa, Blanca, Rojas, Karla, Perez-Severiano, Francisca, Montes, Sergio, Rubio-Osornio, Moises, Guevara, Jorge
Publicada:
1 may 2019
Resumen:
Alzheimer's disease (AD) is a neurodegenerative disorder characterized
by dementia and the aggregation of the amyloid beta peptide (A).
A(25-35) is the most neurotoxic sequence, whose mechanism is associated
with the neuronal death in the Cornu Ammonis 1 (CA1) region of the
hippocampus (Hp) and cognitive damage. Likewise, there are mechanisms of
neuronal survival regulated by heat shock proteins (HSPs). Studies
indicate that pharmacological treatment with flavonoids reduces the
prevalence of AD, particularly epicatechin (EC), which shows better
antioxidant activity. The aim of this work was to evaluate the effect of
EC on neurotoxicity that causes A(25-35) at the level of spatial memory
as well as the relationship with immunoreactivity of HSPs in the CA1
region of the Hp of rats. Our results show that EC treatment reduces the
deterioration of spatial memory induced by the A(25-35), in addition to
reducing oxidative stress and inflammation in the Hp of the animals
treated with EC + A(25-35). Likewise, the immunoreactivity to HSP-60,
-70, and -90 is lower in the EC + A(25-35) group compared to the
A(25-35) group, which coincides with a decrease of dead neurons in the
CA1 region of the Hp. Our results suggest that EC reduces the
neurotoxicity induced by A(25-35), as well as the HSP-60, -70, and -90
immunoreactivity and neuronal death in the CA1 region of the Hp of rats
injected with A(25-35), which favors an improvement in the function of
spatial memory.
Filiaciones:
Diaz, Alfonso:
Benemerita Univ Autonoma Puebla, Fac Ciencias Quim, Puebla 72540, Pue, Mexico
Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Pue. 72540, Mexico
Trevino, Samuel:
Benemerita Univ Autonoma Puebla, Fac Ciencias Quim, Puebla 72540, Pue, Mexico
Pulido-Fernandez, Guadalupe:
Benemerita Univ Autonoma Puebla, Fac Ciencias Quim, Puebla 72540, Pue, Mexico
Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Pue. 72540, Mexico
Martinez-Munoz, Estefania:
Univ Nacl Autonoma Mexico, Fac Med, Dept Bioquim, Ciudad De Mexico 04510, Mexico
Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, 04510, Mexico
Cervantes, Nallely:
Univ Nacl Autonoma Mexico, Fac Med, Dept Bioquim, Ciudad De Mexico 04510, Mexico
Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, 04510, Mexico
Espinosa, Blanca:
Inst Nacl Enfermedades Resp SSA, Dept Bioquim, Ciudad De Mexico 14269, Mexico
Departamento de Bioquímica, Instituto Nacional de Enfermedades Respiratorias, SSA, Ciudad de Mexico, 14269, Mexico
Rojas, Karla:
Univ Valle Mexico, Sede Sur, Dept Ciencias Salud, Psicol, Ciudad De Mexico 04910, Mexico
Departamento de Ciencias de la Salud Psicologia, Universidad del Valle de México, Sede Sur., Ciudad de Mexico, 04910, Mexico
Perez-Severiano, Francisca:
Inst Nacl Neurol SSA, Lab Neurofarmacol Mol & Nanotecnol, Ciudad De Mexico 14269, Mexico
Laboratorio de Neurofarmacología Moleculary Nanotecnología, Instituto Nacional de Neurología, SSA, Ciudad de Mexico, 14269, Mexico
Montes, Sergio:
Inst Nacl Neurol SSA, Dept Neuroquim, Ciudad De Mexico 14269, Mexico
Departamento de Neuroquímica, Instituto Nacional de Neurología, SSA, Ciudad de Mexico, 14269, Mexico
Rubio-Osornio, Moises:
Lab Expt Enfermedades Neurodegenerarivas SSA, Ciudad De Mexico 14269, Mexico
Laboratorio Experimental de Enfermedades Neurodegenerarivas, SSA, Ciudad de Mexico, 14269, Mexico
Guevara, Jorge:
Univ Nacl Autonoma Mexico, Fac Med, Dept Bioquim, Ciudad De Mexico 04510, Mexico
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