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Vinpocetine mitigates aluminum-induced cognitive impairment in socially isolated rats

Author:
Ali, Azza A., Ahmed, Hebatalla I., Khaleel, Sahar A., Abu-Elfotuh, Karema
Source:
Physiology & behavior 2019 v.208 pp. 112571
ISSN:
0031-9384
Subject:
Alzheimer disease, aluminum, anti-inflammatory activity, antioxidants, cerebral cortex, cognitive disorders, forced swimming test, gene expression, glycogen (starch) synthase, hippocampus, histopathology, interleukin-1beta, malondialdehyde, models, necrosis, neoplasms, neuroprotective effect, rats, swimming, tau-protein kinase, tumor necrosis factor-alpha
Abstract:
Several reports have highlighted the role of vinpocetine in Alzheimer's disease (AD). However, the role of vinpocetine in AD under social isolation conditions has not yet been elucidated. Henceforth, this study aimed to investigate the potential neuroprotective effect of vinpocetine in aluminum-induced AD model associated with social isolation. Social isolation increased the escape latency in Morris water maze (MWM) test, elevated the immobility score and decreased swimming score in forced swimming test (FST) in aluminum treated rats. However, vinpocetine enhanced acquisition in MWM test and exerted anti-depressive effect in FST. The histopathological examination showed marked deterioration in the cerebral cortex and hippocampus of AD isolated rats, while vinpocetine revealed overt improvement. In addition, the levels of amyloid-β protein (Aβ), phosphorylated-tau (Ser396), malondialdehyde (MDA), interleukin 1-beta (IL-1β), tumor necrosis alpha (TNFα), p- Glycogen synthase kinase-3β (p-GSK3β) (Tyr216), and β-secretase (BACE1) gene expression were increased in socially isolated aluminum treated rats, yet, vinpocetine treatment reversed these deteriorating effects. Hence, this study provides profound insights into the role of vinpocetine in AD particularly in the conditions of social isolation. The effects of vinpocetine might be attributed not only to its antioxidant and anti-inflammatory properties, but also to its suppressing effect on GSK3β activity and its downstream BACE1.
Agid:
6465621