Effects of (−)-Sesamin on Memory Deficits in MPTP-lesioned Mouse Model of Parkinson's Disease
Natural Product Sciences
;
: 246-251, 2016.
Artigo
em Inglês
| WPRIM
| ID: wpr-146021
ABSTRACT
This study investigated the effects of (−)-sesamin on memory deficits in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse model of Parkinson's disease (PD). MPTP lesion (30 mg/kg/day, 5 days) in mice showed memory deficits including habit learning memory and spatial memory. However, treatment with (−)-sesamin (25 and 50 mg/kg) for 21 days ameliorated memory deficits in MPTP-lesioned mouse model of PD (−)-sesamin at both doses improved decreases in the retention latency time of the passive avoidance test and the levels of dopamine, norepinephrine, 3,4-dihydroxyphenylacetic acid, and homovanillic acid, improved the decreased transfer latency time of the elevated plus-maze test, reduced the increased expression of N-methyl-D-aspartate (NMDA) receptor, and increased the reduced phosphorylation of extracellular signal-regulated kinase (ERK1/2) and cyclic AMP-response element binding protein (CREB). These results suggest that (−)-sesamin has protective effects on both habit learning memory and spatial memory deficits via the dopaminergic neurons and NMDA receptor-ERK1/2-CREB system in MPTP-lesioned mouse model of PD, respectively. Therefore, (−)-sesamin may serve as an adjuvant phytonutrient for memory deficits in PD patients.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Doença de Parkinson
/
Fosforilação
/
Fosfotransferases
/
Ácido 3,4-Di-Hidroxifenilacético
/
Proteínas de Transporte
/
Dopamina
/
Norepinefrina
/
1-Metil-4-Fenil-1,2,3,6-Tetra-Hidropiridina
/
N-Metilaspartato
/
Neurônios Dopaminérgicos
Limite:
Animais
/
Humanos
Idioma:
Inglês
Revista:
Natural Product Sciences
Ano de publicação:
2016
Tipo de documento:
Artigo
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