Protective effects of ginseng on neurological disorders

Abstract

Ginseng (Order: Apiales, Family: Araliaceae, Genus: Panax) has been used as a traditional herbal medicine for over 2000 years, and is recorded to have antianxiety, antidepressant and cognition enhancing properties. The protective effects of ginseng on neurological disorders are discussed in this review. Ginseng species and ginsenosides, and their intestinal metabolism and bioavailability are briefly introduced. This is followed by molecular mechanisms of effects of ginseng on the brain, including glutamatergic transmission, monoamine transmission, estrogen signaling, nitric oxide (NO) production, the Keap1/Nrf2 adaptive cellular stress pathway, neuronal survival, apoptosis, neural stem cells and neuroregeneration, microglia, astrocytes, oligodendrocytes and cerebral microvessels. The molecular mechanisms of the neuroprotective effects of ginseng in Alzheimer's disease (AD) including β-amyloid (Aβ) formation, tau hyperphosphorylation and oxidative stress, major depression, stroke, Parkinson's disease and multiple sclerosis are presented. It is hoped that this discussion will stimulate more studies on the use of ginseng in neurological disorders.

Keywords: brain; ginseng; ginsenoside; glial cells; neurodegeneration; neurons; neuroprotection.

Figure 1

Chemical structure of ginsenosides Rb1 and Rg1. Ginsenoside Rb1 is an example for 20 (S)-PD and ginsenoside Rg1 is an example for 20 (S)-PT type of ginsenosides.

Figure 2

Hypothetical diagram showing the effects of ginseng on signal transduction processes in the brain. phosphatidylcholine (PtdCho); lyso-phosphatidylcholine (lyso-PtdCho); cytosolic phospholipase A2 (cPLA2); arachidonic acid (AA); platelet activating factor (PAF); reactive oxygen species (ROS); Nuclear factor-kappa B (NF-κB); nuclear factor erythroid 2-related factor 2 (Nrf2); cyclooxygenase-2 (COX-2); lipoxygenase (LOX); secretory phospholipase A2 (sPLA2); inducible nitric oxide synthase (iNOS); tumor necrosis factor-α (TNF-α); interleukin-1β (IL-1β); interleukin-6 (IL-6); kelch-like erythroid Cap “n” Collar homologue-associated protein 1 (Keap1); NFE2-related factor 2 (Nrf2); antioxidant response element (ARE); quinine oxidoreductase (QR); hemeoxygenase 1 (HO-1); superoxide dismutase (SOD); glutathione peroxidase (GP); γ-glutamylcysteine ligase (γ-GCL); heat shock proteins (HSPs); amyloid precursor protein (APP); soluble amyloid precursor protein (sAPP); β-amyloid (Aβ); α secretase (ADAM10); and β-secretase (BACE1). This diagram is based on information provided in Choi et al. (2010), Jung et al. (2010), Li et al. (2010), Ye et al. (2011b), Hwang et al. (2012b), Karpagam et al. (2013) and Wang et al. (2013c).