Epigallocatechin gallate protects dopaminergic neurons against 1-methyl-4- phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity by inhibiting microglial cell activation / 南方医科大学学报
Journal of Southern Medical University
; (12): 376-380, 2006.
Article
em En
| WPRIM
| ID: wpr-255306
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WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To observe whether the dopaminergic neuroprotective effect of (-)-epigallocatechin gallate (EGCG) is associated with its inhibition of microglial cell activation in vivo.</p><p><b>METHODS</b>The effects of EGCG at different doses on dopaminergic neuronal survival were tested in a methyl-4-phenyl-pyridinium (MPP+)-induced dopaminergic neuronal injury model in the primary mesencephalic cell cultures. With unbiased stereological method, tyrosine hydroxylase-immunoreactive (TH-ir) cells were counted in the A8, A9 and A10 regions of the substantia nigra (SN) in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated C57BL/6 mice. The effect of EGCG on microglial activation in the SN was also investigated.</p><p><b>RESULTS</b>Pretreatment with EGCG (1 to 100 micromol/L) significantly attenuated MPP+-induced TH-ir cell loss by 22.2% to 80.5% in the mesencephalic cell cultures. In MPTP-treated C57BL/6 mice, EGCG at a low concentration (1 mg/kg) provided significant protection against MPTP-induced TH-ir cell loss by 50.9% in the whole nigral area and by 71.7% in the A9 region. EGCG at 5 mg/kg showed more prominent protective effect than at 1 or 10 mg/kg. EGCG pretreatment significantly inhibited microglial activation and CD11b expression induced by MPTP.</p><p><b>CONCLUSION</b>EGCG exerts potent dopaminergic neuroprotective activity by means of microglial inhibition, which shed light on the potential use of EGCG in treatment of Parkinson's disease.</p>
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Índice:
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Assunto principal:
Doença de Parkinson
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Farmacologia
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Chá
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Mesencéfalo
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Substância Negra
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Dopamina
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Catequina
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Química
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Neuroglia
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Fármacos Neuroprotetores
Limite:
Animals
Idioma:
En
Revista:
Journal of Southern Medical University
Ano de publicação:
2006
Tipo de documento:
Article