Ginsenoside Rb1

Ginsenoside Rb1 promotes the expressions of Nestin, NSE, GFAP and stimulates the differentiation of NSCs^[1]. GRb1 is found to not only inhibit Aβ-induced ROROS overproduction and lipid peroxidation, but also to increase the Bcl-2/Bax ratio and attenuate caspase-3 activation, thereby improving cell survival. GRb1 may therefore act as a ROS scavenger, and such antioxidant properties may play a protective role against Aβ-induced cell injury^[2].

PC12 cells are grown in RPMI-1640 containing 10% heat-inactivated horse serum and 5% fetal bovine serum at 37˚C in a 5% CO2 atmosphere. The medium is changed every other day and cells are plated at the appropriate density according to each experimental scale. To study the effects of GRb1 on Aβ25-35-induced cell injury, cells are pre-incubated with GRb1 for 24 h, and then Aβ25-35 is added to the medium for an additional 24 h. The experimental groups are: A, control; B, 25 μM Aβ25-35; C, 0.01 mM GRb1 + 25 μM Aβ25-35; D, 0.1 mM GRb1 + 25 μM Aβ25-35; E, 1 mM GRb1 + 25 μM Aβ25-35. Following pre-treatment with GRb1 and treatment with Aβ, the cells are subjected to the MTT assay and flow cytometry analysis, the measurement of ROROS and MDADA, Western blotting and immunocytochemistry.

Ginsenoside Rb1 can increase the ability of spatial learning and neural regeneration. It has an anti-neuroinflammatory effect in a rat model of AD. Oral ginsenoside Rb1 can metabolize ginsenoside compound K through intestinal bacteria, and then play a pharmacological role together with esterification of fatty acids to prevent memory loss and improve spatial learning. Ginsenoside Rb1 increases synaptic density and the expression of brain-derived neurotrophic factors Bcl-2 and antioxidant enzyme in hippocampus of mice, and inhibits apoptosis and calcium overload. Ginsenoside Rb1 can stimulate the release of acetylcholine and enhance the expression of choline acetyltransferase mRNA in rat brain, which contributes to the increase of hippocampal neurogenesis. It significantly increased the expression of brain-derived neurotrophic factor (BDNF) in the hippocampus^[1].