Comparable attenuation of Abeta(25-35)-induced neurotoxicity by quercitrin and 17beta-estradiol in cultured rat hippocampal neurons.

In the present work, potential protective effects of quercitrin (a phytoestrogen) on Abeta-induced neurotoxicity in cultured rat hippocampal neurons were investigated in comparison with 17beta-estradiol. Cell viability, oxidative status, and antioxidative potentials were used as comparative parameters. Co-exposure of cultured neurons to Abeta(25-35) with either quercitrin or 17beta-estradiol (50-100 microM) for 72 h attenuated Abeta(25-35)-induced neurotoxicity and lipid peroxidation, but not Abeta(25-35)-induced ROS accumulation. However, only 17beta-estradiol counteracted a reduction in glutathione content and only quercitrin counteracted a reduction in glutathione peroxidase activity. Both compounds displayed no effects on superoxide dismutase activity. A specific estrogen receptor antagonist, ICI 182780, did not abolish neuroprotective effects of quercitrin and 17beta-estradiol. These findings suggested that quercitrin and 17beta-estradiol attenuated Abeta(25-35)-induced neurotoxicity in a comparable manner. Underlying neuroprotective mechanisms of both compounds were probably not related to estrogen receptor-mediated genomic mechanisms but might involve with their antioxidant and free radical scavenging properties.