Neuroprotective Effect of Oxyresveratrol from Smilacis Chinae Rhizome on Amyloid β Protein (25—35)-Induced Neurotoxicity in Cultured Rat Cortical Neurons

抄録

We previously reported that Smilacis chinae rhizome inhibits amyloid β protein (25—35) (Aβ (25—35))-induced neurotoxicity in cultured rat cortical neurons. The present study evaluated the neuroprotective effect of oxyresveratrol isolated from Smilacis chinae rhizome against Aβ (25—35)-induced neurotoxicity on cultured rat cortical neurons. Oxyresveratrol over the concentration range of 1—10 μM significantly inhibited 10 μM Aβ (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 μM) inhibited 10 μM Aβ (25—35)-induced elevation of cytosolic calcium concentration ([Ca²⁺]_c), which was measured by a fluorescent dye, Fluo-4 AM. Oxyresveratrol (1, 10 μM) also inhibited glutamate release into medium and reactive oxygen species (ROS) generation induced by 10 μM Aβ (25—35). These results suggest that oxyresveratrol prevents Aβ (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.