Troxerutin protects hippocampal neurons against amyloid beta-induced oxidative stress and apoptosis
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Date
2017-08-09
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Abstract
Alzheimer’s disease (AD) is an age-related neurodegenerative disease linked with increased production and/or
deposition of amyloid-beta (Aβ) in the brain. The aim of the present study was to investigate the possible neuroprotective
effect of troxerutin on an animal model of Alzheimer's disease. Alzheimer model was induced by a
single dose intracerebroventricular (ICV) injection of Aβ 1–42 (5 nmol/5 μl). Thereafter, troxerutin (300 mg/kg)
was gavaged for 14 days. The hippocampal malondialdehyde (MDA) levels and enzymatic activities of superoxide
dismutase (SOD), glutathione peroxidase (GPx), and acetylcholinesterase (AChE) were measured using enzymelinked
immunosorbent assay (ELISA) method. In addition, the number of apoptotic cells in the dentate gyrus (DG)
was assessed by TUNEL kit. The results showed that ICV microinjection of Aβ 1-42 increased MDA levels, reduced
SOD and GPx, and increased AChE activities in the hippocampus. Chronic administration of troxerutin
significantly attenuated MDA levels and AChE activity and increased SOD and GPx activities in the hippocampus.
Moreover, the number of apoptotic cells was decreased by troxerutin treatment. Taken together, our study demonstrated
that troxerutin could increase the resistance of hippocampal neurons against apoptosis, at least in part, by
diminishing the activity of AChE and oxidative stress. Therefore, troxerutin may have beneficial effects in the
management of Alzheimer's disease.
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Keywords
Alzheimer’s disease, amyloid beta, acetylcholinesterase, oxidative stress