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Prevention of nitric oxide-mediated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease in mice by tea phenolic epigallocatechin 3-gallate.

Choi, JY; Park, CS; Kim, DJ; Cho, MH; Jin, BK; Pie, JE; Chung, WG
Neurotoxicology, 23(3):367-374, 2002
Journal Title
In animal models of Parkinson's disease (PD), the toxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is mediated by oxidative stress, especially by nitric oxide (NO). Inhibition of NO synthase (NOS) activity in the brain produces a neuroprotective effect against PD induced by MPTP Green tea containing high levels of (-)-epigallocatechin 3-gallate (EGCG) was administered to test whether EGCG attenuates MPTP-induced PD in mice through the inhibition of NOS expression. Both tea and the oral administration of EGCG prevented the loss of tyrosine hydroxylase (TH)-positive cells in the substantia nigra (SN) and of TH activity in the striatum. These treatments also preserved striatal levels of dopamine and its metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid (HVA). Both tea and EGCG decreased expressions of nNOS in the substantia nigra. Also tea plus MPTP and EGCG plus MPTP treatments decreased expressions of neuronal NO synthase (nNOS) at the similar levels of EGCG treatment group. Therefore, the preventive effects of tea and EGCG may be explained by the inhibition of nNOS in the substantia nigra.
MeSH terms
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/*antagonists & inhibitors3,4-Dihydroxyphenylacetic Acid/metabolismAnimalsBlotting, WesternCatechin/*analogs & derivatives/*pharmacologyDopamine Agents/*toxicityHomovanillic Acid/metabolismImmunohistochemistryMaleMiceMice, Inbred C57BLNitric Oxide/*physiologyNitric Oxide Synthase/biosynthesisNitric Oxide Synthase Type IParkinson Disease, Secondary/chemically induced/*prevention & controlRNA, Messenger/biosynthesis/geneticsSubstantia Nigra/drug effects/enzymologyTea/*chemistryTyrosine 3-Monooxygenase/metabolism
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Journal Papers > Research Organization > Institute for Medical Sciences
AJOU Authors
진, 병관
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