Campus Units

Biomedical Sciences, Food Science and Human Nutrition

Document Type

Article

Publication Version

Published Version

Publication Date

2015

Journal or Book Title

Parkinson’s Disease

Volume

843906

DOI

10.1155/2015/843906

Abstract

Background. Parkinson’s disease (PD) is a progressive neurodegenerative disease that causes severe brain dopamine depletion. Disruption of iron metabolism may be involved in the PD progression. Objective. To test the protective effect of (−)-epigallocatechin-3-gallate (EGCG) against 6-hydroxydopamine- (6-OHDA-) induced neurotoxicity by regulating iron metabolism in N27 cells. Methods. Protection by EGCG in N27 cells was assessed by SYTOX green assay, MTT, and caspase-3 activity. Iron regulatory gene and protein expression were measured by RT-PCR and Western blotting. Intracellular iron uptake was measured using 55Fe. The EGCG protection was further tested in primary mesencephalic dopaminergic neurons by immunocytochemistry. Results. EGCG protected against 6-OHDA-induced cell toxicity. 6-OHDA treatment significantly () increased divalent metal transporter-1 (DMT1) and hepcidin and decreased ferroportin 1 (Fpn1) level, whereas pretreatment with EGCG counteracted the effects. The increased 55Fe (by 96%, ) cell uptake confirmed the iron burden by 6-OHDA and was reduced by EGCG by 27% (), supporting the DMT1 results. Pretreatment with EGCG and 6-OHDA significantly increased () TH+ cell count (~3-fold) and neurite length (~12-fold) compared to 6-OHDA alone in primary mesencephalic neurons. Conclusions. Pretreatment with EGCG protected against 6-OHDA-induced neurotoxicity by regulating genes and proteins involved in brain iron homeostasis, especially modulating hepcidin levels.

Comments

This article is published as Chen D, Kanthasamy AG, Reddy MB. EGCG protects against 6-OHDA induced neurotoxicity in a cell culture model. Parkinson’s Disease, 2015 (doi:10.1155/2015/843906)

Copyright Owner

Hindawi

Language

en

File Format

application/pdf

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