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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.

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We compared neurotoxicity of piperine and low K+ on cultured cerebellar granule neurons. As considered from lactate dehydrogenase release and 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide reduction, both piperine and shifting from high K+ (25 mM) to low K+ (5.4 mM) were cytotoxic to cerebellar granule neurons. Protein synthesis inhibitors, cycloheximide and anisomycin, and an endonuclease inhibitor, aurintricarboxylic acid, were protective against low K+-induced neuronal death whereas they were ineffective against that induced by piperine. D-alpha-tocopherol, trolox, and a spin trap 3,3,5,5-tetramethyl-1-pyrroline-1-oxide were protective against piperine neurotoxicity whereas they had no effect on that induced by low K+. These results suggest that piperine and low K+ may exert neurotoxic effects on cerebellar granule neurons through different mechanisms. Death of cerebellar granule neurons induced by piperine may be mediated by non-apoptotic mechanisms and may involve membrane lipid peroxidation and/or free radical generation.

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