Abstract
The effect of treatment with melatonin was investigated in a rat model of Alzheimer’s disease (AD) involving a single intra-hippocampal injection of amyloid peptide Aβ1-42. Thirty days after this injection immunohistochemical analysis revealed significant increases of both S-100β and NFκB in cortex and hippocampus of treated animals. Levels of synaptophysin were depressed following treatment and this was confirmed by Western blotting. Histopathological studies revealed a diminution of neuronal cell number in the CA3 area of the hippocampus. Behaviorally, the rate of learning escape from electroshock using a maze box was diminished in Aβ-treated mice. Another group of Aβ treated also received an oral gavage of 0.5 mg/kg melatonin on each of the 30 days between Aβ treatment and sacrifice. The effect of this repeated melatonin exposure was to reverse Aβ-induced changes in CA3 cell number and S-100 levels. The increased cerebral content of NF-κB and the behavioral changes caused by Aβ treatment were partially reversed by melatonin. However, melatonin administration had no effect on the reduced level of synaptophysin in Aβ-treated mice. Overall, these findings suggest that melatonin may exert a potentially beneficial effect upon the progression of AD.
Keywords: Alzheimer's disease, amyloid, hippocampus, learning, melatonin, NF-κB.
Current Aging Science
Title:Melatonin Decreases Levels of S100β and NFκB, Increases Levels of Synaptophysinina Rat Model of Alzheimer's Disease
Volume: 6 Issue: 2
Author(s): Zhou Jun, Zhou Li, Wang Fang, Yang Fengzhen, Wen Puyuan, Li Wenwen, Song Zhi and Stephen C. Bondy
Affiliation:
Keywords: Alzheimer's disease, amyloid, hippocampus, learning, melatonin, NF-κB.
Abstract: The effect of treatment with melatonin was investigated in a rat model of Alzheimer’s disease (AD) involving a single intra-hippocampal injection of amyloid peptide Aβ1-42. Thirty days after this injection immunohistochemical analysis revealed significant increases of both S-100β and NFκB in cortex and hippocampus of treated animals. Levels of synaptophysin were depressed following treatment and this was confirmed by Western blotting. Histopathological studies revealed a diminution of neuronal cell number in the CA3 area of the hippocampus. Behaviorally, the rate of learning escape from electroshock using a maze box was diminished in Aβ-treated mice. Another group of Aβ treated also received an oral gavage of 0.5 mg/kg melatonin on each of the 30 days between Aβ treatment and sacrifice. The effect of this repeated melatonin exposure was to reverse Aβ-induced changes in CA3 cell number and S-100 levels. The increased cerebral content of NF-κB and the behavioral changes caused by Aβ treatment were partially reversed by melatonin. However, melatonin administration had no effect on the reduced level of synaptophysin in Aβ-treated mice. Overall, these findings suggest that melatonin may exert a potentially beneficial effect upon the progression of AD.
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Cite this article as:
Jun Zhou, Li Zhou, Fang Wang, Fengzhen Yang, Puyuan Wen, Wenwen Li, Zhi Song and Bondy C. Stephen, Melatonin Decreases Levels of S100β and NFκB, Increases Levels of Synaptophysinina Rat Model of Alzheimer's Disease, Current Aging Science 2013; 6 (2) . https://dx.doi.org/10.2174/18746098112059990005
DOI https://dx.doi.org/10.2174/18746098112059990005 |
Print ISSN 1874-6098 |
Publisher Name Bentham Science Publisher |
Online ISSN 1874-6128 |
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