Protective effect of ginsenoside Rb1 on beta-amyloid protein(1-42)-induced neurotoxicity in cortical neurons.

The effects of ginsenosides were thought to prevent neurodegenerative processes associated with aging. The accumulation of beta-amyloid protein (Abeta) within the brain is one of the pathological hallmarks of Alzheimer's disease (AD). There is no one effective treatment of AD. To investigate the effects of ginsenoside Rb1 (GRb1) on neuronal damage induced by Abeta and potential mechanisms of the effects of GRb1 in vitro, morphological observation and biochemical analysis combining primary cultured neurons were adopted. A positive control was pre-treated with Trolox. Neurons that were treated with Abeta 1-42 (2 muM) were shrunken perikaryon with loss of neurite processes; the survival rate of neurons decreased almost to 50% (p<0.01). Lactate dehydrogenase (LDH) release, malondialdehyde (MDA) product and superoxide dismutase (SOD) activity level all increased obviously (p<0.01 or p<0.05). However, neurons pre-treated with GRb1 (0.1, 1 and 10 muM) or Trolox (10 muM) had a survival rate increase compared with neurons treated with Abeta alone; LDH release and MDA product decreased distinctly, and the increase in SOD activity in Abeta-treated neurons was attenuated evidently (p<0.01 or p<0.05). Thus, we conclude that GRb1 exerted neuroprotection obviously. GRb1 protected neurons against the toxicity of Abeta, most likely through an antioxidant pathway. GRb1 could be useful neuroprotective agents of AD.