摘要：Our previous studies reported that methanol extract of Sanguisorbae radix from Sanguisorba officinalis L. (Rosaceae) prevented neuronal cell damage induced by Aβ (25—35) in vitro . The present study was carried out to investigate the effect of gallic acid isolated from Sanguisorbae radix on Aβ (25—35)-induced neurotoxicity using cultured rat cortical neurons. Gallic acid (0.1, 1 μ M ) showed a concentration-dependent inhibition on Aβ (25—35) (10 μ 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 μ M Aβ (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 μ M Aβ (25—35), which was measured by HPLC. These results suggest that gallic acid prevents Aβ (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.
