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Brain Behav Immun ; 73: 282-293, 2018 10.
Article in English | MEDLINE | ID: mdl-29782911

ABSTRACT

Estrogen is well known to have a preventative effect in Alzheimer's disease (AD) pathology. Several studies have demonstrated that nuclear factor kappa-B (NF-ĸB) can contribute to the effects of estrogen on the development of AD. We investigated whether NF-ĸB affects amyloid-beta (Aß)-induced memory impairment in an estrogen-lacking condition. In the present study, nine-week-old Institute cancer research (ICR) mice were ovariectomized to block estrogen stimulation. Ten weeks after the ovariectomization, mice were administered with Aß (300 pmol) via intracerebroventricular (ICV) infusion for 2 weeks. Memory impairment, neuroinflammatory protein expression, and amyloidogenic pathways were then measured. Ovariectomized mice demonstrated severe memory impairment, Aß accumulation, neprilysin downregulation, and activation of NF-ĸB signaling compared to sham-control mice. In vitro experiments demonstrated that ß-estradiol (10 µM) inhibited Aß (1 µM)-induced neuroinflammation in microglial BV-2 cells and prevented Aß-induced cell death in primary cultured neuronal cells. As in in vivo experiments, NF-ĸB activation was significantly upregulated in in vitro experiments. Furthermore ß-estradiol treatment inhibited NF-ĸB activation in both of microglial BV-2 cells and cultured neuronal cells. These findings suggest that estrogen may protect against memory impairment through the regulation of Aß accumulation and neurogenic inflammation by inhibiting NF-κB activity.


Subject(s)
Amyloid beta-Peptides/metabolism , Estrogens/physiology , Memory Disorders/metabolism , Alzheimer Disease/metabolism , Amyloid beta-Peptides/physiology , Animals , Astrocytes/metabolism , Cyclooxygenase 2/metabolism , Estradiol/pharmacology , Estrogens/deficiency , Estrogens/metabolism , Female , Glial Fibrillary Acidic Protein/metabolism , Inflammation/metabolism , Lipopolysaccharides/pharmacology , Memory Disorders/physiopathology , Mice , Mice, Inbred ICR , Microglia/metabolism , NF-kappa B/metabolism , Neuroimmunomodulation/immunology , Nitric Oxide Synthase Type II/metabolism , Ovariectomy/methods , Primary Cell Culture , Signal Transduction/drug effects
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