Non-ginsenoside nicotinic activity in ginseng species.

Amongst the many different therapeutic applications of ginseng are beneficial effects on age-related cognitive impairments. Ageing in the brain is associated with a loss of nicotinic receptor binding and receptor stimulation increases binding. Stimulation of the CNS (central nervous system) nicotinic receptor is considered to be beneficial in relation to symptomatic treatment and neuroprotection in age-associated cognitive disorders which involve a further receptor loss. We assessed Panax ginseng, Panax quinquefolium and several chemical constituents of these plants for nicotinic activity based on displacement of 3H-(-)nicotine from human brain cerebral cortex membranes in vitro. Dose-dependent displacement was evident in crude ethanol extracts of Panax ginseng and Panax quinquefolium. Assay of an extract of Panax ginseng showed the plant to have affinity for both the nicotinic receptor, and to a lesser extent the muscarinic receptor (IC50 2.12 mg/mL and 5.25 mg/mL respectively). Activity was largely conserved after the extraction of choline and other water soluble quaternary ammonium compounds (QAC), indicating that the activity of the plant extracts was not due to choline. Displacement binding assay of some purified chemical constituents, including a number of ginsenosides, showed that these were not primarily responsible for Panax activity. The active chemical constituent has yet to be identified, but the demonstrated nicotinic activity of ginseng warrants further investigation with reference to therapeutic activity in age-related conditions such as dementia.