Antioxidative stress effect of epicatechin and catechin induced by Aβ25-35in rats and use of the electrostatic potential and the Fukui function as a tool to elucidate specific sites of interaction.
Alzheimer's disease (AD) is a neurodegenerative disorder caused by the aggregation of the amyloid-beta peptide (Aβ) in senile plaques and cerebral vasculature. The Aβ25-35fraction has shown the most toxicity; its neurotoxic mechanisms are associated with the generation of oxidative stress and reactive astrogliosis that induce neuronal death and memory impairment. Studies indicate that pharmacological treatment with flavonoids reduces the rate of AD, in particular, it has been shown that antioxidants are compounds that could interact with this peptide due to their antioxidant proprieties. In this study, experimental and computational tools were used to calculate the molecular electrostatic potential and the Fukui function with the Gaussian 09 computational program, to predict the most reactive parts of these molecules and make the complex between Aβ25-35and two flavonoids (catechin and epicatechin) in the absolute gas-phase, where a possible interaction between them was observed. This is important for understanding the Aβ25-35-Flavonoid (A-F) interaction as a therapeutic strategy to inhibit the neurotoxic effects that this peptide causes in AD, which currently is still considered an ambiguous process.
Departamento de Fisicomatematicas, Facultad de Ciencias Químicas Benemérita Universidad Autónoma de Puebla, Av. San Claudio y 14 Sur, Col. San Manuel, Puebla, Pue. 72570, Mexico.
Trinidad
T
Cruz-González
Laboratorio Experimental de Enfermedades Neurodegenrativas, Instituto Nacional de Neurología y Neurocirugía, Manuel Velasco Suárez, 14269 Mexico City, Mexico.
Estephania
E
Cortez-Torres
Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía, Manuel Velasco Suárez, 14269 Mexico City, Mexico.
Francisca
F
Perez-Severiano
Departamento de Bioquímica, Instituto Nacional de Enfermedades Respiratorias, Mexico, D.F., Mexico.
Blanca
B
Espinosa
Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City, Mexico.
Jorge
J
Guevara
Departamento de Química Organica, Facultad de Ciencias Químicas, Benemérita, Universidad Autónoma de Puebla, Av. San Claudio y 14 Sur, Col. San Manuel, Puebla, Pue. 72570, Mexico.
Aarón
A
Perez-Benitez
Lab. de Química Teórica, Centro de Investigación, Dpto. de Fisicoquímica, Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Edif. 105-I, San Claudio y 22 Sur, Ciudad Universitaria, Col. San Manuel, Puebla, Puebla 72570, Mexico.
Francisco J
FJ
Melendez
Departamento de Farmacia, Facultad de Ciencias Químicas Benemérita Universidad Autónoma de Puebla, Av. San Claudio y 14 Sur, Col. San Manuel, Puebla, Pue. 72570, Mexico. Electronic address: alfonso.diaz@correo.buap.mx.
Alfonso
A
Díaz
Departamento de Fisicomatematicas, Facultad de Ciencias Químicas Benemérita Universidad Autónoma de Puebla, Av. San Claudio y 14 Sur, Col. San Manuel, Puebla, Pue. 72570, Mexico. Electronic address: ramses.ramirez@correo.buap.mx.
Ramsés E
RE
Ramírez
D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D002392:Catechin / Q000494:pharmacology*; D016923:Cell Death / Q000187:drug effects; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects*; D010446:Peptide Fragments / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D055672:Static Electricity
D016229:Amyloid beta-Peptides; D000975:Antioxidants; D018696:Neuroprotective Agents; D010446:Peptide Fragments; D017382:Reactive Oxygen Species; C074636:amyloid beta-protein (25-35); D002392:Catechin
Amyloid- β(25–35); Astrocytes; Electrostatic potential; Flavonoid compounds; Hippocampus; Oxidative stress