Depression is one of the most commonly diagnosed neuropsychiatric diseases, but the underlying mechanism and medicine are not well-known. Although Panax (P.) ginseng has been reported to exert protective effects in various neurological studies, little information is available regarding its antidepressant effects.

Orally administered ginsengs come in contact with the gut microbiota and their hydrophilic constituents, such as ginsenosides, are metabolized to hydrophobic compounds by gastric juice and gut microbiota: protopanxadiol-type ginsenosides are mainly transformed into compound K and ginsenoside Rh2, protopanaxatriol-type ginsenosides are to ginsenoside Rh1 and protopanaxatriol, and ocotillol-type ginsenosides to ocotillol. Although this metabolizing activity varies between individuals, the metabolism of ginsenosides to compound K by gut microbiota in individuals treated with ginseng is proportional to the area under the blood concentration curve (AUC) for compound K in their blood samples.

Recent studies have shown that Korean Red Ginseng (KRG) successfully protects against dopaminergic neuronal death in the nigrostriatal pathway of a Parkinson’s disease (PD) mouse model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration; however, the mechanism has yet to be identified. Therefore, in this study we used 2-dimensional electrophoresis (2-DE) to investigate the effects of KRG on the changes in protein expression in the substantia nigra (SN) of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice.