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Epigallocatechin gallate induces extracellular degradation of amyloid β-protein by increasing neprilysin secretion from astrocytes through activation of ERK and PI3K pathways.

Abstract：

:Amyloid-β (Aβ) production and clearance in the brain is a crucial focus of investigations into the pathogenesis of Alzheimer disease. Imbalance between production and clearance leads to accumulation of Aβ. The important Aβ-degrading enzymes in the brain are neprilysin (NEP) and insulin-degrading enzyme (IDE), and defective enzyme expression may facilitate Aβ deposition in sporadic late-onset AD patients. It has been suggested that epigallocatechin gallate (EGCG), a member of the catechin family, might be an effective treatment for AD, because it has been shown to elevate NEP expression. Therefore, we examined whether catechins, which are functional components of common foods, could regulate the degradation of Aβ by inducing NEP and IDE expression. We also investigated the role of catechins in activating intracellular signal transduction in astrocytes. Treatment of cultured rat astrocytes with EGCG significantly reduced the expression of NEP, but not IDE, in a concentration- and time-dependent manner. NEP expression in cultured astrocytes was suppressed by activation of extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3K), and reduced NEP expression was accompanied by an increase of NEP release into the extracellular space (culture medium). Moreover, culture medium from EGCG-treated astrocytes facilitated the degradation of exogenous Aβ. These results suggest that EGCG may have a beneficial effect on AD by activating ERK-and PI3K-mediated pathways in astrocytes, thus increasing astrocyte secretion of NEP and facilitating degradation of Aβ.

journal_name

Neuroscience

journal_title

Neuroscience

authors

Yamamoto N,Shibata M,Ishikuro R,Tanida M,Taniguchi Y,Ikeda-Matsuo Y,Sobue K

doi

10.1016/j.neuroscience.2017.08.030

subject

Has Abstract

pub_date

2017-10-24 00:00:00

pages

70-78

eissn

0306-4522

issn

1873-7544

pii

S0306-4522(17)30596-1

journal_volume

362

pub_type

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