Epigallocatechin-3-gallate prevents systemic inflammation-induced memory deficiency and amyloidogenesis via its anti-neuroinflammatory properties

Title
Epigallocatechin-3-gallate prevents systemic inflammation-induced memory deficiency and amyloidogenesis via its anti-neuroinflammatory properties
Author(s)
최동영이영중[이영중]윤여표[윤여표]한상배[한상배]오기완[오기완]홍진태[홍진태]
Keywords
AMYLOID PRECURSOR PROTEIN; GALLATE EGCG PREPARATIONS; GREEN TEA POLYPHENOL; LIPOPOLYSACCHARIDE-INDUCED-NEUROINFLAMMATION; INTERCELLULAR-ADHESION MOLECULE-1; INDUCED MICROGLIAL ACTIVATION; STIMULATING FACTOR-RECEPTOR; ALZHEIMER TRANSGENIC MICE; IN-VIVO MODELS; MOUSE MODEL
Issue Date
201301
Publisher
ELSEVIER SCIENCE INC
Citation
JOURNAL OF NUTRITIONAL BIOCHEMISTRY, v.24, no.1, pp.298 - 310
Abstract
Neuroinflammation has been known to play a critical role in the pathogenesis of Alzheimer's disease (AD) through amyloidogenesis. In a previous study, we found that systemic inflammation by intraperitoneal (ip) injection of lipopolysaccharide (LPS) induces neuroinflammation and triggers memory impairment. In this present study, we investigated the inhibitory effects of epigallocatechin-3-gallate (EGCG) on the systemic inflammation-induced neuroinflammation and amyloidogenesis as well as memory impairment. ICR mice were orally administered with EGCG (1.5 and 3 mg/kg) for 3 weeks, and then the mice were treated by ip injection of LPS (250 mu g/kg) for 7 days. We found that treatment of LPS induced memory-deficiency-like behavior and that EGCG treatment prevented LPS-induced memory impairment and apoptotic neuronal cell death. EGCG also suppressed LPS-induced increase of the amyloid beta-peptide level and the expression of the amyloid precursor protein (APP), beta-site APP cleaving enzyme 1 and its product C99. In addition, we found that EGCG prevented LPS-induced activation of astrocytes and elevation of cytokines including tumor necrosis factor-alpha, interleukin (IL)-1 beta, macrophage colony-stimulating factor, soluble intercellular adhesion molecule-1 and IL-16, and the increase of inflammatory proteins, such as inducible nitric oxide synthase and cyclooxygenase-2, which are known factors responsible for not only activation of astrocytes but also amyloidogenesis. In the cultured astrocytes, EGCG also inhibited LPS-induced cytokine release and amyloidogenesis. Thus, this study shows that EGCG prevents memory impairment as well as amyloidogenesis via inhibition of neuroinflammatory-related cytokines released from astrocytes and suggests that EGCG might be a useful intervention for neuroinflammation-associated AD. (c) 2013 Elsevier Inc. All rights reserved.
URI
http://hdl.handle.net/YU.REPOSITORY/26766http://dx.doi.org/10.1016/j.jnutbio.2012.06.011
ISSN
0955-2863
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약학대학 > 약학부 > Articles
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