期刊
BRAIN RESEARCH
卷 1250, 期 -, 页码 164-174出版社
ELSEVIER
DOI: 10.1016/j.brainres.2008.10.012
关键词
(-)-Epigallocatechin-3-gallate (EGCG); Lipopolysaccharide (LPS); Neuroinflammation; Alzheimer's disease (AD)
资金
- Korea Research Foundation
- Korean Government (MOEHRD)
- LG Household Healthcare
Neuroinflammation has been known to play a role in the pathogenesis of AD. Our previous study showed that lipopolysaccharide (LPS) induced memory impairment through the accumulation of A beta via the increase of beta- and gamma-secretase. In this study, we investigated the possible preventive effect of (-)-epigallocatechin-3-gallate (EGCG) on memory deficiency caused by LPS through the inhibition of A beta(1-42) generation. Oral treatment with EGCG (1.5 and 3 mg/kg, for 3 weeks) into drinking water ameliorated LPS (1 mu g/mouse, i.c.v.)-induced memory deficiency in a dose dependent manner. In addition, EGCG also dose-dependently inhibited LPS-induced elevation of A beta level through attenuation of LPS-induced beta- and gamma-secretase activities and expression of its metabolic products; C99 and A beta. Moreover, EGCG prevented LPS-induced neuronal cell death as well as the expression of inflammatory proteins, inducible nitric oxide synthetase and cyclooxygenase-2. This study therefore suggests that EGCG prevents LPS-mediated apoptotic cell death through the inhibition of the elevation of A beta via the inhibition of beta- and gamma-secretases, and thus EGCG can be a useful agent against neuroinflammation-associated development or progression of AD. (C) 2008 Elsevier B.V. All rights reserved.
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