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J Korean Neurol Assoc. 2005 Dec;23(6):806-813. Korean. Original Article.
Youn YC .
Department of Neurology, Chung-Ang University College of Medicine, Seoul, Korea. neudoc@cau.ac.kr
Abstract

BACKGROUND: Considerable evidences suggest that the beta-amyloid acts as a neurotoxin, and the epigallocatechin-3- gallate (EGCG) has the anti-inflammatory and anti-oxidant properties. The purpose of this study was to investigate whether the EGCG reduces the death of the cultured hippocampal tissues exposed to the beta-amyloid 1-42 fragments (A beta1-42). METHOD: We cultured the hippocampus of postnatal 7 days old Sprague-Dawley rat into slices of 450 micrometer. The tissue slices had been exposed with 100 micro M A beta1-42 at an interval of 3 days since 12 DIV (days in vitro). Following co-treatment of the tissue with 10 micro M EGCG and A beta1-42, we evaluated EGCG effect on A beta1-42 induced neurotoxicity by measuring the expression of Bcl-2 and NeuN protein and by morphological observation of the hippocampus slice cultures with propidium iodide (PI) and bromodeoxyuridine (BrdU) staining. RESULTS: The EGCG exerted a significant role in restoration of NeuN protein expression inhibited by A beta1-42, showed inhibitory effects fluorescence in PI stained tissues, and increased the anti-BrdU stained cell. CONCLUSIONS: 10 micro M EGCG reduced the A beta1-42 induced neurotoxicity of the hippocampus slice culture.

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