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

Abstract

Alzheimers disease (AD) is a brain disease attributed to the accumulation of extracellular senile plaques comprising {beta}-amyloid peptide (A{beta}). In this study, a transgenic Caenorhabditis elegans containing the human beta amyloid A{beta}42 gene which exhibited paralysis when expressed, was used to study the anti-paralysis effect of salvianolic acid A. Various concentrations ranging from 1 g/ml to 100 g/ml of salvianolic acid A were tested and exhibited the highest effect on the worm at the concentration of 100 g/ml. For anti-aggregation effect, 14 g/ml salvianolic acid A (within 4 mg/ml of Danshen) showed a significant level of inhibition of the formation of A{beta} fibrils. An amount of 100 g/ml of salvianolic acid A had the potential in reducing the 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 A{beta}42 aggregation and decreased A{beta}-induced oxidative stress.