Antioxidant effects of epicatechin on the hippocampal toxicity caused by amyloid-beta 25-35 in rats.
Amyloid-beta is involved in neurodegeneration in Alzheimer's disease. The Amyloid-beta fraction 25-35 (Amyloid-beta 25-35) is believed to cause neurotoxicity through oxidative stress. We evaluated the antioxidant effects of Epicatechin on the Abeta25-35-caused hippocampal toxicity in vivo. Biochemical and histological evaluations, and learning and memory tasks, were assessed. Amyloid-beta 25-35 (100 microM/microL) or vehicle was injected into the CA1 hippocampal region of the rat 5 h after a single oral dose of Epicatechin (30 mg/kg). Lipid peroxidation and reactive oxygen species formation were measured in Amyloid-beta- and Amyloid-beta-Epicatechin-treated groups at 2 h and 24 h after dosing and formation of the lesion. There was an increase in lipid peroxidation and reactive oxygen species formation at 2-h and 24-h postlesion. Learning and memory tests were made 27-30 days after surgery in independent groups under the same experimental conditions. Immunohistochemical detection of glial-fibrilar acidic protein (GFAP) was evaluated in hippocampal tissues from the animals 30-days postsurgery. Amyloid-beta 25-35 caused a significant increase in lipid peroxidation and reactive oxygen species and a decrease in memory skills. In addition, hippocampal tissues from Amyloid-beta 25-35-treated animals showed an increased immunoreactivity against GFAP. In contrast, animals pretreated with Epicatechin had a significant decrease in lipid peroxidation and reactive oxygen species and an improvement in memory skills. GFAP immunoreactivity was also decreased. Our results showed that Amyloid-beta 25-35-caused oxidative damage of the hippocampus was blocked by the administration of Epicatechin.
Cuevas
Elvis
E
Laboratorio Experimental de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía, Mexico, DF 14269, Mexico.
Limón
Daniel
D
Pérez-Severiano
Francisca
F
Díaz
Alfonso
A
Ortega
Laura
L
Zenteno
Edgar
E
Guevara
Jorge
J
D016229:Amyloid beta-Peptides / Q000633:toxicity*; D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology*; D002392:Catechin / Q000378:metabolism / Q000494:pharmacology*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism; D007150:Immunohistochemistry; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D008568:Memory / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D010446:Peptide Fragments / Q000633:toxicity*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism
D016229:Amyloid beta-Peptides; D000975:Antioxidants; D005904:Glial Fibrillary Acidic Protein; D010446:Peptide Fragments; D017382:Reactive Oxygen Species; C074636:amyloid beta-protein (25-35); D002392:Catechin