Ginsenosides Rbl and Rg3 Attenuate Glutamate-induced Neurotoxicity in Primary Cultures of Rat Cortical Cells

  • Kim, Young-C. (College Pharmacy, Seoul National University) ;
  • Kim, So.R. (College Pharmacy, Seoul National University) ;
  • Markelonis, George J. (Department of Anatomy and Neurobiology, University of Maryland, School of Medicine) ;
  • Oh, Tae-H. (Department of Anatomy and Neurobiology, University of Maryland, School of Medicine)
  • Published : 1998.06.01

Abstract

In the present study, we assayed a number of compounds isolated from Panax ginseng C. A. Meyer (Araliaceae) for an ability to protect rat cortical cell cultures from the deleterious effects of the neurotoxicant, glutamate. We found that ginsenosides Rbl and Rg3 significantly attenuated glutamate-induced neurotoxicity. Brief exposure of cultures to excess glutamate caused extensive neuronal death. Glutamate-induced neuronal cell damage was significantly reduced by pretreatment with Rbl and Rgl. Ginsenosides Rbl and Rg3 inhibited the overproduction of nitric oxide which routinely follows glutamate neurotoxicity and preserved the level of superoxide dismutase in glutamate-treated cells. Furthermore, in cultures treated with glutamate, these ginsenosides inhibited the formation of malondialdehyde, a compound produced during lipid peroxidation, and diminished the influx of calcium. These results show that ginsenosides Rbl and Rg1 exerted significant neuroprotective effects on cultured cortical cells. As such, these compounds may be efficacious in protecting neurons from oxidative damage produced by exposure to excess glutamate.

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