Oxidative stress has been implicated as a primary cause of neuronal death in certain neurodegenerative disorders and in aging brains. Natural products have been used in Asian societies for centuries for treating such neurodegenerative disorders as senile dementia. In an effort to identify active neu
Arctigenin protects cultured cortical neurons from glutamate-induced neurodegeneration by binding to kainate receptor
✍ Scribed by Young P. Jang; So R. Kim; Young H. Choi; Jinwoong Kim; Sang G. Kim; George J. Markelonis; Tae H. Oh; Young C. Kim
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- English
- Weight
- 414 KB
- Volume
- 68
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
Abstract
We previously reported that arctigenin, a lignan isolated from the bark of Torreya nucifera, showed significant neuroprotective activity against glutamate‐induced toxicity in primary cultured rat cortical cells. In this study, the mode of action of arctigenin was investigated using primary cultures of rat cortical cells as an in vitro system. Arctigenin significantly attenuated glutamate‐induced neurotoxicity when added prior to or after an excitotoxic glutamate challenge. The lignan protected cultured neuronal cells more selectively from neurotoxicity induced by kainic acid than by N‐methyl‐D‐aspartate. The binding of [^3^H]‐kainate to its receptors was significantly inhibited by arctigenin in a competitive manner. Furthermore, arctigenin directly scavenged free radicals generated by excess glutamate and successfully reduced the level of cellular peroxide in cultured neurons. These results suggest that arctigenin exerted significant neuroprotective effects on glutamate‐injured primary cultures of rat cortical cells by directly binding to kainic acid receptors and partly scavenging of free radicals. © 2002 Wiley‐Liss, Inc.
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