Neurological

Analgesia Intraperitoneal administration of ginsenoside Rf has been shown to potentiate opioid-induced analgesia in mice. Furthermore, ginsenosides prevented tolerance to the opiate that was not associated with opioid or GABA receptors (Nemmani & Ramarao 2003).

Neuroprotection Ginseng saponins have demonstrated dose-dependent neuroprotective activity in vitro and in vivo (Kim et al 2005b). Ginsenosides Rb1 and © 2007 Elsevier Australia

Rg 1 have a partial neurotrophic and neuroprotective role in dopaminergic cell cultures (Radad et al 2004) and Rg3 has been shown to inhibit chemically induced injuries in hippocampal neurons (Kim et al 2002b). Pretreatment with ginsenosides (50 or 100 mg/kg IP for 7 days) has been shown to be neuroprotective in vivo (Lee et al 2002a). An in vitro survival assay demonstrated that ginsenosides Rb1 and Rg1 protect spinal cord neurons against damage. The ginsenosides protect spinal neurons from excitotoxicity induced by glutamate and kainic acid, as well as oxidative stress induced by H202. The optimal doses are 20-40 micromol/L for ginsenosides Rb1 and Rg 1 (Liao et al 2002). The lipophilic fraction of ginseng has been shown to induce differentiation of neurons and promote neuronal survival in the rat cortex. The effect is thought to be mediated via protein-kinase-C-dependent pathways (Mizumaki et al 2002).

It has been suggested that the neuroprotective effects of ginseng against hypoperfusion/reperfusion induced brain injury demonstrated in animal models, suggests a potential for use in CVD (Shah et al 2005). Cognitive function Following oral consumption, the active metabolites of protopanaxadiol saponins may reactivate neuronal function in Alzheimer's disease according to in vivo evidence (Komatsu et al 2005). Ginseng also enhances the survival of newly generated neurons in the hippocampus which may contribute to the purported benefits of ginseng for improving learning tasks (Qiao et al 2005). Anticonvulsant Pretreatment (30 minutes) with 100 mg/kg ginseng significantly protected rats against pentylenetetrazole-induced seizures (Gupta et al 2001).

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