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Effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice

The present study aimed to evaluate the cinnamic acid effect on memory impairment, oxidative stress, and cholinergic dysfunction in streptozotocin (STZ)-induced diabetic model in mice. In this experimental study, 48 male Naval Medical Research Institute (NMRI) mice (30–35 g) were chosen and were ran...

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Autores principales: Hemmati, Ali Asghar, Alboghobeish, Soheila, Ahangarpour, Akram
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Physiological Society and The Korean Society of Pharmacology 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5928339/
https://www.ncbi.nlm.nih.gov/pubmed/29719448
http://dx.doi.org/10.4196/kjpp.2018.22.3.257
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author Hemmati, Ali Asghar
Alboghobeish, Soheila
Ahangarpour, Akram
author_facet Hemmati, Ali Asghar
Alboghobeish, Soheila
Ahangarpour, Akram
author_sort Hemmati, Ali Asghar
collection PubMed
description The present study aimed to evaluate the cinnamic acid effect on memory impairment, oxidative stress, and cholinergic dysfunction in streptozotocin (STZ)-induced diabetic model in mice. In this experimental study, 48 male Naval Medical Research Institute (NMRI) mice (30–35 g) were chosen and were randomly divided into six groups: control, cinnamic acid (20 mg/kg day, i.p. ), diabetic, and cinnamic acid-treated diabetic (10, 20 and 40 mg/kg day, i.p. ). Memory was impaired by administering an intraperitoneal STZ injection of 50 mg/kg. Cinnamic acid was injected for 40 days starting from the 21st day after confirming STZ-induced dementia to observe its therapeutic effect. Memory function was assessed using cross-arm maze, morris water maze and passive avoidance test. After the administration, biochemical parameters of oxidative stress and cholinergic function were estimated in the brain. Present data indicated that inducing STZ caused significant memory impairment, whereas administration of cinnamic acid caused significant and dose-dependent memory improvement. Assessment of brain homogenates indicated cholinergic dysfunction, increase in lipid peroxidation and reactive oxygen species (ROS) levels, and decrease in glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities in the diabetic group compared to the control animals, whereas cinnamic acid administration ameliorated these indices in the diabetic mice. The present study demonstrated that cinnamic acid improves memory by reducing the oxidative stress and cholinergic dysfunction in the brain of diabetic mice.
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spelling pubmed-59283392018-05-01 Effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice Hemmati, Ali Asghar Alboghobeish, Soheila Ahangarpour, Akram Korean J Physiol Pharmacol Original Article The present study aimed to evaluate the cinnamic acid effect on memory impairment, oxidative stress, and cholinergic dysfunction in streptozotocin (STZ)-induced diabetic model in mice. In this experimental study, 48 male Naval Medical Research Institute (NMRI) mice (30–35 g) were chosen and were randomly divided into six groups: control, cinnamic acid (20 mg/kg day, i.p. ), diabetic, and cinnamic acid-treated diabetic (10, 20 and 40 mg/kg day, i.p. ). Memory was impaired by administering an intraperitoneal STZ injection of 50 mg/kg. Cinnamic acid was injected for 40 days starting from the 21st day after confirming STZ-induced dementia to observe its therapeutic effect. Memory function was assessed using cross-arm maze, morris water maze and passive avoidance test. After the administration, biochemical parameters of oxidative stress and cholinergic function were estimated in the brain. Present data indicated that inducing STZ caused significant memory impairment, whereas administration of cinnamic acid caused significant and dose-dependent memory improvement. Assessment of brain homogenates indicated cholinergic dysfunction, increase in lipid peroxidation and reactive oxygen species (ROS) levels, and decrease in glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities in the diabetic group compared to the control animals, whereas cinnamic acid administration ameliorated these indices in the diabetic mice. The present study demonstrated that cinnamic acid improves memory by reducing the oxidative stress and cholinergic dysfunction in the brain of diabetic mice. The Korean Physiological Society and The Korean Society of Pharmacology 2018-05 2018-04-25 /pmc/articles/PMC5928339/ /pubmed/29719448 http://dx.doi.org/10.4196/kjpp.2018.22.3.257 Text en Copyright © Korean J Physiol Pharmacol http://creativecommons.org/licenses/by-nc/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Hemmati, Ali Asghar
Alboghobeish, Soheila
Ahangarpour, Akram
Effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice
title Effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice
title_full Effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice
title_fullStr Effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice
title_full_unstemmed Effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice
title_short Effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice
title_sort effects of cinnamic acid on memory deficits and brain oxidative stress in streptozotocin-induced diabetic mice
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5928339/
https://www.ncbi.nlm.nih.gov/pubmed/29719448
http://dx.doi.org/10.4196/kjpp.2018.22.3.257
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