American Journal of Chinese Medicine 2009-01-01

Inhibition of NMDA receptors underlies the neuroprotective effect of ginsenoside Rb3.

Liang-Liang Peng, Hong-Mei Shen, Zheng-Lin Jiang, Xia Li, Guo-Hua Wang, Yun-Feng Zhang, Kai-Fu Ke

Index: Am. J. Chin. Med. 37(4) , 759-70, (2009)

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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.