Cellular and Molecular Neurobiology

, Volume 32, Issue 1, pp 121–128

Ginsenoside Rd Protects Neurons Against Glutamate-Induced Excitotoxicity by Inhibiting Ca2+ Influx

Authors

  • Chen Zhang
    • Department of Neurology, Xijing HospitalThe Fourth Military Medical University
  • Fang Du
    • Department of Neurology, Xijing HospitalThe Fourth Military Medical University
    • Department of Neurology, Xijing HospitalThe Fourth Military Medical University
  • Ruidong Ye
    • Department of Neurology, Xijing HospitalThe Fourth Military Medical University
  • Haoran Cheng
    • Department of Neurology, Xijing HospitalThe Fourth Military Medical University
    • Lin Tong Air Force Aeromedical Training Institute
  • Junliang Han
    • Department of Neurology, Xijing HospitalThe Fourth Military Medical University
  • Lei Ma
    • Department of Neurology, Xijing HospitalThe Fourth Military Medical University
  • Rong Cao
    • Institute of NeurosciencesThe Fourth Military Medical University
  • Zhiren Rao
    • Institute of NeurosciencesThe Fourth Military Medical University
    • Department of Neurology, Xijing HospitalThe Fourth Military Medical University
Original Research

DOI: 10.1007/s10571-011-9742-x

Cite this article as:
Zhang, C., Du, F., Shi, M. et al. Cell Mol Neurobiol (2012) 32: 121. doi:10.1007/s10571-011-9742-x

Abstract

Our previous studies have demonstrated that ginsenoside Rd (GSRd), one of the principal ingredients of Pana notoginseng, has neuroprotective effects against ischemic stroke. However, the possible mechanism(s) underlying the neuroprotection of GSRd is/are still largely unknown. In this study, we treated glutamate-injured cultured rat hippocampal neurons with different concentrations of GSRd, and then examined the changes in neuronal apoptosis and intracellular free Ca2+ concentration. Our MTT assay showed that GSRd significantly increased the survival of neurons injured by glutamate in a dose-dependent manner. Consistently, TUNEL and Caspase-3 staining showed that GSRd attenuated glutamate-induced cell death. Furthermore, calcium imaging assay revealed that GSRd significantly attenuated the glutamate-induced increase of intracellular free Ca2+ and also inhibited NMDA-triggered Ca2+ influx. Thus, the present study demonstrates that GSRd protects the cultured hippocampal neurons against glutamate-induced excitotoxicity, and that this neuroprotective effect may result from the inhibitory effects of GSRd on Ca2+ influx.

Keywords

Ginsenoside RdGlutamateExcitotoxicityCalcium influxNMDA receptor

Copyright information

© Springer Science+Business Media, LLC 2011