Neuroprotective Properties of Gallic Acid from Sanguisorbae Radix on Amyloid .BETA. Protein (25-35)-Induced Toxicity in Cultured Rat Cortical Neurons

Abstract

Our previous studies reported that methanol extract of Sanguisorbae radix from Sanguisorba officinalis L. (Rosaceae) prevented neuronal cell damage induced by Abeta (25-35) in vitro. The present study was carried out to investigate the effect of gallic acid isolated from Sanguisorbae radix on Abeta (25-35)-induced neurotoxicity using cultured rat cortical neurons. Gallic acid (0.1, 1 microM) showed a concentration-dependent inhibition on Abeta (25-35) (10 microM)-induced apoptotic neuronal death, as assessed by a 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33,342 staining. Pretreatment of gallic acid inhibited 10 microM Abeta (25-35)-induced elevation of cytosolic Ca(2+) concentration ([Ca(2+)](c)) and generation of reactive oxygen species (ROS), which were measured by fluorescent dyes. Gallic acid also inhibited glutamate release into medium induced by 10 microM Abeta (25-35), which was measured by HPLC. These results suggest that gallic acid prevents Abeta (25-35)-induced apoptotic neuronal death by interfering with the increase of [Ca(2+)](c), and then by inhibiting glutamate release and generation of ROS, and that these effects of gallic acid may be partly associated with the neuroprotective effect of Sanguisorbae radix.