Ginsenoside Rd Attenuates A Beta(25-35)-Induced Oxidative Stress And Apoptosis In Primary Cultured Hippocampal Neurons

One of the most common pathological changes in Alzheimer's disease (AD) brain is the large number of amyloid beta (A beta) peptides accumulating in lesion areas. Ginsenosides are the most active components extracted from ginseng. Ginsenoside Rd (GRd) is a newly discovered saponin that has a stronger pharmacological activity than other ginsenosides, especially in neuroprotection. Here we examined the neuroprotective effects of GRd against neuronal insults induced by A beta(25-35) in primary cultured hippocampal neurons. A 10 mu M GRd treatment significantly prevented the loss of hippocampal neurons induced by A beta(25-35). In addition, GRd significantly ameliorated A beta(25-35)-induced oxidative stress by decreasing the reactive oxygen species (ROS) production and malondialdehyde (MDA) level, and increasing the levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px); which is similar in treatments with 10 mu M of probucol (PB) and 100 mu M of edaravone (EDA). Moreover, our present study demonstrated that GRd significantly enhanced the expression of Bcl-2 mRNA, and decreased the expressions of Bax mRNA and Cyt c mRNA. GRd also downregulated the protein level of cleaved Caspase-3 compared to controls. These results highlighted the neuroprotective effects of GRd against A beta(25-35)-induced oxidative stress and neuronal apoptosis, suggesting that this may be a promising therapeutics against AD. (C) 2015 Elsevier Ireland Ltd. All rights reserved.