Effects of salvianolic acid A on β-amyloid mediated toxicity in Caenorhabditis elegans model of Alzheimer's disease

Alzheimer’s disease (AD) is a brain disease attributed to the accumulation of extracellular senile plaques comprising β-amyloid peptide (Aβ). In this study, a transgenic Caenorhabditis elegans ( C. elegans ) containing the human beta amyloid Aβ 42 gene which exhibited paralysis when expressed, was used to study the anti-paralysis effect of salvianolic acid A. Various concentrations ranging from 1 μg/ml to 100 μg/ml of salvianolic acid A were tested which exhibited the highest effect on the worm at the concentration of 100 μg/ml. For anti-aggregation effect, 14 μg/ml of salvianolic acid A (within 4 mg/ml of Danshen) showed a significant level of inhibition of the formation of Aβ fibrils. An amount of 100 μg/ml of salvianolic acid A had the potential in reducing the reactive oxygen species (ROS) but did not totally obliterate the ROS production in the worms. Salvianolic acid A was found to delay the paralysis of the transgenic C. elegans , decrease Aβ 42 aggregation and decrease Aβ-induced oxidative stress.