Sanguisorbae radix and its active component, gallic acid, protect amyloid β protein (25–35)-induced neurotoxicity

Sanguisorbae Radix from Sanguisorba officinalis L. (Rosacea) is widely used in Korea and China due to its various pharmacological activities [1],[2]. The present study investigated the effect of the methanol extract of SR and gallic acid, which was isolated as an active component from SR by an activity-guided purification, on amyloid β protein (25–35) (Aβ (25–35)), a synthetic 25–35 amyloid peptide, -induced neurotoxicity using primarily cultured rat cortical neurons. SR (10 to 50µg/ml) and gallic acid (0.1 and 1µM), inhibited Aβ (25–35) (10µM)-induced neuronal cell death, as assessed by a 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and the number of apoptotic nuclei, evidenced by Hoechst 33342 staining. Pretreatment of SR and gallic acid inhibited 10µM Aβ (25–35)-induced elevation of cytosolic calcium concentration ([Ca2+]c), which was measured by a fluorescent dye, fluo-4 AM. SR and gallic acid inhibited glutamate release into medium induced by 10µM Aβ (25–35), which was measured by HPLC, and generation of reactive oxygen species. Data were expressed as mean±SEM and statistical significance was assessed by one-way analysis of variance (ANOVA) with subsequent Tukey's tests. These results suggest that SR and gallic acid prevent Aβ (25–35)-induced neuronal cell damage by interfering with the increase of [Ca2+]c, and then by inhibiting glutamate release, generation of ROS. Furthermore, these effects of gallic acid may be associated with the neuroprotective effect of SR.