Ginsenoside Rb1 protects PC12 cells against β-amyloid-induced cell injury

Abstract

Excessive accumulation of beta-amyloid (A beta) has been proposed as a pivotal event in the pathogenesis of Alzheimer's disease. Possible mechanisms underlying A beta-induced neuronal cytotoxicity include oxidative stress and apoptosis. Reactive oxygen species (ROS) have been proposed to be involved in the apoptotic mechanism of A beta-induced cytotoxicity. Ginsenoside Rb1 (GRb1), which is among the key compounds of ginsenoside, found in ginseng, may be a potent scavenger of ROS. To examine the potential protective effect of GRb1 in A beta(25-35)-induced cytotoxicity, cells were pre-treated with GRb1 for 24 h, and then A beta(25-35) was added to the medium for an additional 24 h. Exposure to A beta led to the accumulation of ROS and lipid peroxidation, eventually causing a decrease in the Bcl-2/ Bax ratio, caspase-3 activation, cell apoptosis and cell death. Pre-treatment with GRb1 not only inhibited A beta-induced ROS overproduction and lipid peroxidation, but also increased the Bcl-2/Bax ratio and attenuated 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 A beta-induced cell injury. Further exploration of GRb1 antioxidant properties may provide novel therapeutic strategies for the treatment of Alzheimer's disease.