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Epicatechin Reduces Spatial Memory Deficit Caused by Amyloid-β25–35 Toxicity Modifying the Heat Shock Proteins in the CA1 Region in the Hippocampus of Rats

1
Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, Pue. PC. 72540, Mexico
2
Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México PC. 04510, Mexico
3
Departamento de Bioquímica, Instituto Nacional de Enfermedades Respiratorias, SSA, Ciudad de Mexico, PC. 14269, Mexico
4
Departamento de Ciencias de la Salud, Psicologia. Universidad del Valle de México, sede Sur., Ciudad de Mexico, PC. 04910, Mexico
5
Laboratorio de Neurofarmacología Molecular y Nanotecnología, Instituto Nacional de Neurología, SSA, Ciudad de Mexico, PC. 14269, Mexico
6
Departamento de Neuroquímica, Instituto Nacional de Neurología, SSA, Ciudad de Mexico, PC. 14269, Mexico
7
Laboratorio Experimental de Enfermedades Neurodegenerarivas, SSA, Ciudad de Mexico, PC. 14269, Mexico
*
Author to whom correspondence should be addressed.
Antioxidants 2019, 8(5), 113; https://doi.org/10.3390/antiox8050113
Received: 8 February 2019 / Revised: 25 March 2019 / Accepted: 1 April 2019 / Published: 30 April 2019
(This article belongs to the Special Issue Antioxidant Activity of Polyphenolic Plant Extracts)
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Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by dementia and the aggregation of the amyloid beta peptide (Aβ). Aβ25–35 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 Aβ25–35 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 Aβ25–35, in addition to reducing oxidative stress and inflammation in the Hp of the animals treated with EC + Aβ25–35. Likewise, the immunoreactivity to HSP-60, -70, and -90 is lower in the EC + Aβ25–35 group compared to the Aβ25–35 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 Aβ25–35, as well as the HSP-60, -70, and -90 immunoreactivity and neuronal death in the CA1 region of the Hp of rats injected with Aβ25–35, which favors an improvement in the function of spatial memory. View Full-Text
Keywords: reactive oxygen species; proinflammatory cytokines; Alzheimer’s disease reactive oxygen species; proinflammatory cytokines; Alzheimer’s disease
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Diaz, A.; Treviño, S.; Pulido-Fernandez, G.; Martínez-Muñoz, E.; Cervantes, N.; Espinosa, B.; Rojas, K.; Pérez-Severiano, F.; Montes, S.; Rubio-Osornio, M.; Guevara, J. Epicatechin Reduces Spatial Memory Deficit Caused by Amyloid-β25–35 Toxicity Modifying the Heat Shock Proteins in the CA1 Region in the Hippocampus of Rats. Antioxidants 2019, 8, 113.

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