On page 427 of the article referenced above, under the heading Assessment of Neurotoxicity in the Materials and Methods section, the formula given for the assessment of percentage cell viability was printed incorrectly. The formula is correctly stated in a footnote to Table on page 429. The correct
Ginsenosides Rb1and Rg3protect cultured rat cortical cells from glutamate-induced neurodegeneration
β Scribed by Young C. Kim; So R. Kim; George J. Markelonis; Tae H. Oh
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 72 KB
- Volume
- 53
- Category
- Article
- ISSN
- 0360-4012
No coin nor oath required. For personal study only.
β¦ Synopsis
Certain natural products and Asian herbal remedies have been used in Asia to attenuate neurodegenerative diseases, including senile dementia. We have examined derivatives of several natural products for potential neuroprotective activity in an in vitro test system. In the present study, we assayed a number of compounds that were 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 Rb 1 and Rg 3 significantly attenuated glutamateinduced neurotoxicity. Brief exposure of cultures to excess glutamate caused extensive neuronal death. Glutamate-induced neuronal cell damage was reduced significantly by pretreatment with Rb 1 and Rg 3 . Ginsenosides Rb 1 and Rg 3 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 that is produced during lipid peroxidation, and diminished the influx of calcium. These results show that ginsenosides Rb 1 and Rg 3 exerted significant neuroprotective effects on cultured cortical cells. Therefore, these compounds may be efficacious in protecting neurons from oxidative damage that is produced by exposure to excess glutamate.
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