Neuroprotective effect of oxyresveratrol from Smilacis chinae rhizome on amyloid β protein (25-35)-induced neurotoxicity in cultured rat cortical neurons

We previously reported that Smilacis chinue rhizome inhibits amyloid beta protein (25-35) (A beta (25-35))-induced neurotoxicity in cultured rat cortical neurons. The present study evaluated the neuroprotective effect of oxyresveratrol isolated from Smilacis chinae rhizome against A beta (25-35)-induced neurotoxicity on cultured rat cortical neurons. Oxyresveratrol over the concentration range of 1-10 mu M significantly inhibited 10 mu M A beta (25-35)-induced neuronal cell death, which was measured by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. Oxyresveratrol (10 mu M) inhibited 10 mu M A beta (25-35)-induced elevation of cytosolic calcium concentration ([Ca2+](c)), which was measured by a fluorescent dye, Fluo-4 AM. Oxyresveratrol (1, 10 mu M) also inhibited glutamate release into medium and reactive oxygen species (ROS) generation induced by 10 mu M A beta (25-35). These results suggest that oxyresveratrol prevents A beta (25-35)-induced neuronal cell damage by interfering with the increase of [Ca2+](c), and then by inhibiting glutamate release and ROS generation. Furthermore, these effects of oxyresveratrol may be associated with the neuroprotective effect of Smilacis chinae rhizome.