Repository of Research and Investigative Information

Repository of Research and Investigative Information

Hormozgan University of Medical Sciences

How sodium arsenite improve amyloid beta-induced memory deficit?

(2016) How sodium arsenite improve amyloid beta-induced memory deficit? PHYSIOLOGY & BEHAVIOR.

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Official URL: https://www.sciencedirect.com/science/article/pii/...

Abstract

Abstract Evidence has shown that arsenic exposure, besides its toxic effects results in impairment of learning and memory, but its molecular mechanisms are not fully understood. In the present study, we examined sodium arsenite (1, 5, 10, 100 nM) effects on contextual and tone memory of male rats in Pavlovian fear conditioning paradigm alone and in co-administration with beta-amyloid. We detected changes in the level of caspase-3, nuclear factor kappa-B (NF-kappa B), cAMP response element-binding (CREB), heme oxygenase-1 and NF-E2-related factor-2 (Nrf2) by Western blot. Sodium arsenite in high doses induced significant memory impairment 9 and 16 days after infusion. By contrast, low doses of sodium arsenite attenuate memory deficit in A beta injected rats after 16 days. Our data revealed that treatment with high concentration of sodium arsenite increased caspase-3 cleavage and NF-kappa B level, 9 days after injection. Whereas, low doses of sodium arsenite cause Nrf2 and HO-1 activation and increased CREB phosphorylation in the hippocampus. These findings suggest the concentration dependent effects of sodium arsenite on contextual and tone memory. Moreover, it seems that the neuroprotective effects of ultra low concentrations of sodium arsenite on A beta-induced memory impairment is mediated via an increase Nrf2, HO-1 and CREB phosphorylation levels and decrease caspase-3 and NF-kappa B amount. (C) 2016 Published by Elsevier Inc.

Item Type: Article
Keywords: Sodium arsenite; Alzheimer's disease; Amyloid beta; Nrf2; Oxidative stress; CREB NF-KAPPA-B; ALZHEIMERS-DISEASE; CELL-PROLIFERATION; HEME OXYGENASE-1; MONOMETHYLARSONOUS ACID; CREB PHOSPHORYLATION; INDUCED APOPTOSIS; OXIDATIVE STRESS; EPITHELIAL-CELLS; GENE-EXPRESSION
Subjects: QT Physiology > QT104-172 Human Physiology
QV Pharmacology > QV 701-835 Pharmacy and Pharmaceutics
Depositing User: مهندس هدی فهیم پور
URI: http://eprints.hums.ac.ir/id/eprint/5031

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