Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 616, Issue 1-3, Pages 122-127Publisher
ELSEVIER
DOI: 10.1016/j.ejphar.2009.06.013
Keywords
Alzheimer's disease; Epicatechin; Flavonoid; Amyloid-beta; Oxidative stress; Memory
Categories
Funding
- CONACYT [61205]
- INNN [15/06]
- UNAM PAPIIT [IN214609, IN212108]
- Laboratory of Neuropharmacology-BUAP [LNAB1-08]
- Programa Universitario de Epidermiologia, Genomica y proteomica [SDEI.PTID.05.1]
- Facultad de Medicina, UNAM
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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 AB25-35-caused hippocampal toxicity in vivo. Biochemical and histological evaluations, and learning and memory tasks, were assessed. Amyloid-beta 25-35 (100 mu M/mu L) 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 Amyloidbeta 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 Amyloidbeta 25-35-caused oxidative damage of the hippocampus was blocked by the administration of Epicatechin. (C) 2009 Elsevier B.V. All rights reserved.
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