Comparable Attenuation of Aβ25–35-Induced Neurotoxicity by Quercitrin and 17β-Estradiol in Cultured Rat Hippocampal Neurons

被引:13
作者
Sadudee Rattanajarasroj
Surachai Unchern
机构
[1] Chulalongkorn University,Department of Pharmacology and Physiology, Faculty of Pharmaceutical Sciences
来源
Neurochemical Research | 2010年 / 35卷
关键词
Quercitrin; 17β-estradiol; Aβ; Neurotoxicity; Neuroprotection; Hippocampal neurons;
D O I
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中图分类号
学科分类号
摘要
In the present work, potential protective effects of quercitrin (a phytoestrogen) on Aβ-induced neurotoxicity in cultured rat hippocampal neurons were investigated in comparison with 17β-estradiol. Cell viability, oxidative status, and antioxidative potentials were used as comparative parameters. Co-exposure of cultured neurons to Aβ25–35 with either quercitrin or 17β-estradiol (50–100 μM) for 72 h attenuated Aβ25–35-induced neurotoxicity and lipid peroxidation, but not Aβ25–35-induced ROS accumulation. However, only 17β-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 17β-estradiol. These findings suggested that quercitrin and 17β-estradiol attenuated Aβ25–35-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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页码:1196 / 1205
页数:9
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