Neuroprotective properties of gallic acid from Sanguisorbae radix on amyloid β protein (25-35)-induced toxicity in cultured rat cortical neurons

Our previous studies reported that methanol extract of Sanguisorbae radix from Sanguisorba officinails L. (Rosaceae) prevented neuronal cell damage induced by A beta (25-35) in vitro. The present study was carried out to investigate the effect of gallic acid isolated from Sanguisorbae radix on A beta (25-35)-induced neurotoxicity using cultured rat cortical neurons. Gallic acid (0.1, 1 mu M) showed a concentration-dependent inhibition on A beta (25-35) (10 mu M)-induced apoptotic neuronal death, as assessed by a 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. Pretreatment of gallic acid inhibited 10 mu M A beta (25-35)-induced elevation of cytosolic Ca2+ concentration ([Ca2+](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 mu M A beta (25-35), which was measured by HPLC. These results suggest that gallic acid prevents A beta (25-35)induced apoptotic neuronal death by interfering with the increase of [Ca2+](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.