Ginseng, a perennial plant belonging to the Panax genus of the Araliaceae family, has been used in China, Korea, and Japan as a traditional herbal medicine for thousands of years. Ginseng is recorded to have exhibited a wide variety of beneficial pharmacological effects and has become a popular and worldwide known health supplement and drug. The protective effects of ginseng on central nervous system are discussed in this review. Ginseng species and ginsenosides and their intestinal metabolism and bioavailability are concisely introduced. The molecular mechanisms of the effects of ginseng on central nervous system, mainly focused on the neuroprotection properties of ginseng, memory, and learning enhanced properties, and the effects on neurodegenerative disorders are presented. Thus, ginseng and its constituents are of potential merits in the treatment of cerebral disorders.

Background:Ginseng has been used as an ergogenic agent, although evidence for its effectiveness is weak. A randomized, double-blind, placebo-controlled clinical trial was conducted to evaluate the effect of a ginsenoside complex (UG0712) on changes in exercise performance.

Methods:Sedentary individuals (  117) were randomly assigned into one of three groups: low-dose ginsenoside supplementation (100 mg/d,  39), high-dose ginsenoside supplementation (500 mg/d,  39), or a placebo group (500 mg/d,  39). All participants underwent a supervised 12-wk aerobic and resistance exercise training course. To assess the effects of supplementation on physical performance, maximal oxygen consumption (VOmax), anaerobic threshold (AT), lactic acid, and muscle strength of the dominant knee were measured at baseline, every visit, and after the training program.

Results:Both ginsenoside groups showed significant increases in VOmax and muscular strength during exercise training. There were no definite changes in AT and lactic acid levels over time. After exercise training, there were definite differences in the VOmax (28.64.9 to 33.7 ± 4.9 ml/kg/min in high-dose group vs. 30.4 ± 6.7 to 32.8 ± 6.6 ml/kg/min in placebo,  0.029) and AT (19.3 ± 4.2 to 20.9 ± 3.5 ml/kg/min in high-dose group vs. 20.0 ± 5.1 to 20.0 ± 4.9 ml/kg/min in placebo,  0.038) between the high-dose ginsenoside and placebo groups. However, there was no difference in VOmax between the low-dose ginsenoside and placebo groups (  0.254). There were no differences in muscular strength during exercise training among the three groups.

Conclusion:High-dose ginsenoside supplementation (UG0712) augmented the improvement of aerobic capacity by exercise training.

Emerging evidence indicates exercise training could mediate mitochondrial quality control through the improvement of mitochondrial dynamics. Ginsenoside Rg3 (Rg3), one of the active ingredients in Panax ginseng, is well known in herbal medicine as a tonic and restorative agent. However, the molecular mechanism underlying the beneficial effects of Rg3 has been elusive. In the present study, we compared the effects of Rg3 administration with aerobic exercise on mitochondrial adaptation in cardiac muscle tissue of Sprague-Dawley (SD) rats. Three groups of SD rats were studied: (1) sedentary control, (2) Rg3-treated and (3) aerobic exercise trained. Both aerobic exercise training and Rg3 supplementation enhanced peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1α) and nuclear factor-E2-related factor 2 (Nrf2) protein levels in cardiac muscle. The activation of PGC-1α led to increased mRNA levels of mitochondrial transcription factor A (Tfam) and nuclear related factor 1(Nrf1), these changes were accompanied by increases in mitochondrial DNA copy number and complex protein levels, while activation of Nrf2 increased levels of phase II detoxifying enzymes, including nicotinamide adenine dinucleotide phosphate:quinone oxidoreductase 1(NQO1), superoxide dismutase (MnSOD) and catalase. Aerobic exercise also enhanced mitochondrial autophagy pathway activity, including increased conversion of LC3-I to LC3-II and greater expression of beclin1 and autophagy-related protein 7 (ATG7), these effects of aerobic exercise are comparable to that of Rg3. These results demonstrate that Rg3 mimics improved cardiac adaptations to exercise by regulating mitochondria dynamic remodeling and enhancing the quantity and quality of mitochondria.

Ginseng, the root of Panax ginseng C.A. Meyer (Araliaceae), is a widely used herbal medicine. Ginsenosides, the active ingredients of ginseng, are the main components responsible for many beneficial actions of ginseng. In the present study, we tested 10 different ginsenosides in the previously developed in vitro Huntington's disease (HD) assay with primary medium spiny striatal neuronal cultures (MSN) from the YAC128 HD mouse model. We found that nanomolar concentrations of ginsenoside Rb1 and Rc effectively protected YAC128 medium spiny neurons from glutamate-induced apoptosis and that Rg5 was protective at micromolar concentration. The other seven ginsenosides tested were not effective or exerted toxic effects in MSN cultures. From further experiments, we suggested that neuroprotective effects of ginsenosides Rb1, Rc, and Rg5 could correlate with their ability to inhibit glutamate-induced Ca(2+) responses in cultured MSN. From these results we concluded that ginsenosides Rb1, Rc, and Rg5 offer a potential therapeutic choice for the treatment of HD and possibly other neurodegenerative disorders. (c) 2009 Wiley-Liss, Inc.