Inhibition of NMDA receptors underlies the neuroprotective effect of ginsenoside Rb3.
Am J Chin Med
; 37(4): 759-70, 2009.
Article
em En
| MEDLINE
| ID: mdl-19655413
ABSTRACT
In order to investigate the mechanisms underlying the neuroprotective effect of ginsenoside Rb3, rat hippocampal neurons were primarily cultured, and exposed to 1 mM N-methyl-D-aspartate (NMDA), cell viability and lactate dehydrogenase leakage were measured. Ca2+ influx was determined by calcium imaging with a laser confocal microscopy. The influences of ginsenoside Rb3 on these variables were examined. Patch-clamp technique was used to observe the effects of ginsenoside Rb3 on NMDA-evoked current. The results show that treatment of Rb3 raised the neuronal viability, reduced the leakage of lactate dehydrogenase, and inhibited NMDA-elicited Ca2+ influx in a dose-dependent manner. In the presence of Rb3, NMDA-evoked peak current was inhibited, and Ca2+-induced desensitization of NMDA current was facilitated. It is suggested that ginsenoside Rb3 could exert a neuroprotective role on hippocampal neurons, a role which was partly mediated by the facilitation of Ca2+-dependent deactivation of NMDA receptors, and the resultant reduction of intracellular free Ca2+ level.
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Base de dados:
MEDLINE
Assunto principal:
Receptores de N-Metil-D-Aspartato
/
Fármacos Neuroprotetores
/
Ginsenosídeos
/
Neurônios
Idioma:
En
Revista:
Am J Chin Med
Ano de publicação:
2009
Tipo de documento:
Article
País de afiliação:
China