4.3 Article

Epigallocatechin-3-gallate and curcumin suppress amyloid beta-induced beta-site APP cleaving enzyme-1 upregulation

期刊

NEUROREPORT
卷 19, 期 13, 页码 1329-1333

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/WNR.0b013e32830b8ae1

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A beta; beta-site APP cleaving enzyme-1; curcumin; epigallocatechin-3-gallate; neuron-glia co-culture; radical oxygen species

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Beta-site APP cleaving enzyme-1 (BACE-1), is a rate-limiting enzyme for beta amyloid production. Beta amyloid induces the production of radical oxygen species and neuronal injury. Oxidative stress plays a key role in various neurological diseases such as ischemia and Alzheimer's disease. Recent studies suggest that oxidative stress induces BACE-1 protein upregulation in neuronal cells. Here, we demonstrate that naturally occurring compounds ( - )-epigallocatechin-3-gallate and curcumin suppress beta amyloid-incluced BACE-1 upregulation. Exposure of beta amyloid 1-42 to neuronal culture increased BACE-1 protein levels. ( - )- Epigallocatechin-3-gallate or curcumin significantly attenuated beta amyloid-incluced radical oxygen species production and beta-sheet structure formation. These two compounds have novel pharmacological effects that may be beneficial for Alzheimer's disease treatment. NeuroReport 19:1329-1333 (c) 2008 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

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