The effects of the total saponin of Dipsacus asperoides on the damage of cultured neurons induced by beta-amyloid protein 25-35.

According to the pathogenesis of Alzheimer's disease (AD), beta-amyloid protein (A beta) was directly toxic to neurons, leading to neurodegeneration. Total saponin of Dipsacus asperoides (tSDA) is one of the main ingredients of Dipsacus asperoide, a traditional Chinese medicine. To explore the effects of tSDA on neuronal damage induced by A beta in vitro, biochemical analysis combining primary cultured neurons were adopted. Neurons were treated with 35 mmol/L A beta for 24 h, and tSDA at concentrations of 1-300 mg/L were added to A beta-treated cultures 24 h in advance, A beta for 24 h, the survival rate of neurons decreased closely by 50%. Lactate dehydrogenase release and the Malondialdehyde (MDA) level increased substantially. However, if neurons were pretreated with tSDA, the survival rate of neurons was higher than A beta-treated alone. Lactate dehydrogenase release and the MDA level decreased distinctly. Results demonstrated that tSDA possessed a neuroprotective action and that tSDA protected neurons against the toxicity of A beta, most likely by relieving oxidative stress or inhibiting the process of A beta, inducing free radical generation.