Antioxidant effects of Epicatechin on the hippocampal toxicity caused by Amyloid-beta 25-35 in rats

• DOI: 10.1016/j.ejphar.2009.06.013
• Publication Date: 2009-06-19T04:22:55Z
• Authors: Elvis Cuevas; Daniel Limón; Francisca Pérez-S...; Alfonso Díaz; Laura Ortega; Edgar Zenteno; Jorge Guevara
• Keywords: Male; 0303 health sciences; Amyloid beta-Peptides; Hippocampus; Immunohistochemistry; Antioxidants; Catechin; Peptide Fragments; Rats; 3. Good health; Oxidative Stress; 03 medical and health sciences; Memory; Glial Fibrillary Acidic Protein; Animals; Gliosis; Lipid Peroxidation; Rats, Wistar; Maze Learning; Reactive Oxygen Species

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.