Involvement of N-Methyl-D-Aspartic Acid Receptor and DL-α-Amino-3-Hydroxy-5- Methyl-4-Isoxazole Propionic Acid Receptor in Ginsenosides Rb1 and Rb3 against Oxygen-Glucose Deprivation-Induced Injury in Hippocampal Slices from Rat

Abstract

Objective: Ginsenosides, Rb1 and Rb3, are the major protopanaxadiol components of ginseng saponin. In the present study, the influences of ginsenosides Rb1 and Rb3 on N-methyl-D-aspartic acid (NMDA) receptor or DL-α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor-mediated synaptic transmission after oxygen-glucose deprivation (OGD) were investigated. Methods: NMDA receptor population spike (NMDA-PS) or AMPA receptor-mediated population spike (AMPA-PS) was recorded in the CA1 pyramidal cell layer of rat hippocampal slices by electrophysiological techniques. Results: Under normal conditions, ginsenosides Rb3 and Rb1 depressed glutamate receptors-mediated synaptic transmission. Fourteen min of OGD resulted in a poor recovery amplitude of NMDA-PS or AMPA-PS after reoxygenation. Ginsenoside Rb3 significantly delayed the appearance of transient recovery of PS during OGD, and improved the recovery amplitudes of NMDA-PS and AMPA-PS after reoxygenation. However, the similar protective effects of ginsenoside Rb1 were observed only on NMDA-PS but not AMPA-PS. Conclusion: These results suggest that ginsenosides Rb1 and Rb3 have the different inhibitions on NMDA and AMPA receptors-mediated response, which may partially explain the different protective effects of these agents on ischemic neuronal death.

A mini-review on pharmacological effects of ginsenoside Rb3, a marked saponin from Panax genus

“…G-Rb3 exhibits neuroprotection via modulating GABA A receptor in the OGD model in vitro (Jiang et al, 2011). In addition to this receptor, the neuroprotective activity of G-Rb3 was reported through the inhibitory action on the NMDA receptor (Jiang et al, 2018). In NMDA receptortreated rat hippocampal neurons cells, neuronal viability was reduced accompanied by the leakage of LDH and Ca 2+ influx (Berliocchi et al, 2005;White et al, 2000).…”

The Untapped Potential of Ginsenosides and American Ginseng Berry in Promoting Mental Health via the Gut–Brain Axis

“…Such neuroprotective mechanisms occur through varied antioxidant effects, such as suppressing inducible nitric oxide synthase in hypoxic hippocampal neurons [60], preserving superoxide dismutase (SOD) and catalase (CAT) levels [61], and inducing Nrf2 transcription activity [62], which is downregulated in neurological conditions, such as depression [63]. Likewise, ginsenoside Rb3 was shown to interact with multiple neurotransmitters and receptors, leading to neuroprotective effects through inhibiting the NMDA receptor [64,65], activating the GABA(A) receptor [66], or acting beneficially on the noradrenergic pathway to relieve depression in rodent models [55,67].…”