Reciprocal activity of ginsenosides in the production of proinflammatory repertoire, and their potential roles in neuroprotection in vivo.

Ginsenosides, the active compounds inherent to most Ginseng species [e. g., Panax ginseng (Araliaceae)], have recently been the focus of increased attention, due to both their purported CNS, antineoplastic and immunomodulatory effects, and their ability to stimulate phagocytosis. In this study, we attempted to determine the effects of ginsenosides Rb1 and Rg1 in a rat model, with specific emphasis on nitric oxide and cytokines, which have been implicated in chronic brain inflammation. We discovered that Rb1 and Rg1 exert opposite effects in a dose-dependent manner (50-250 microg/mL). Whereas Rg1 stimulated nitric oxide and proinflammatory cytokines (IL-1beta, IL-6, and TNF-alpha), Rb1 exerted a significant inhibitory effect on this proinflammatory repertoire. In addition, the genetic expression of bcl-2 and bax, both of which have been implicated in apoptosis, was regulated by treatment with Rb1 and Rg1, at a concentration of 250 microg/mL. Moreover, when combined treatment with equal doses of Rb1 and Rg1 was given, Rb1 significantly counteracted the stimulatory effects of Rg1, as evidenced by an NO assay. This effect persisted stably for 72 h. In conclusion, neurodegenerative diseases such as Alzheimer's disease, which is caused primarily by cell death due to chronic inflammation and cell stress, might be controlled by proper doses of non-toxic, natural Rg1 and Rb1.