This study investigated the neuroprotective activity of red ginseng extract (RGE, Panax ginseng, C. A. Meyer) against kainic acid-\r\n(KA-) induced excitotoxicity in vitro and in vivo. In hippocampal cells, RGE inhibited KA-induced excitotoxicity in a dosedependent\r\nmanner as measured by the MTT assay. To study the possible mechanisms of the RGE-mediated neuroprotective\r\neffect against KA-induced cytotoxicity, we examined the levels of intracellular reactive oxygen species (ROS) and [Ca2+]i in\r\ncultured hippocampal neurons and found that RGE treatment dose-dependently inhibited intracellular ROS and [Ca2+]i elevation.\r\nOral administration of RGE (30 and 200 mg/kg) in mice decreased the malondialdehyde (MDA) level induced by KA injection\r\n(30 mg/kg, i.p.). In addition, similar results were obtained after pretreatment with the radical scavengers Trolox and N, N-\r\ndimethylthiourea (DMTU). Finally, after confirming the protective effect of RGE on hippocampal brain-derived neurotropic\r\nfactor (BDNF) protein levels, we found that RGE is active compounds mixture in KA-induced hippocampal mossy-fiber function\r\nimprovement. Furthermore, RGE eliminated 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals, and the IC50 was approximately\r\n10 mg/ml. The reductive activity of RGE, as measured by reaction with hydroxyl radical (ââ?¬Â¢OH), was similar to trolox. The secondorder\r\nrate constant of RGE for ââ?¬Â¢OH was 3.5ââ?¬â??4.5 Ã?â?? 109M-1Ã?·S-1. Therefore, these results indicate that RGE possesses radical\r\nreduction activity and alleviates KA-induced excitotoxicity by quenching ROS in hippocampal neurons
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