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Neuroprotective effect of thymoquinone in acrylamide-induced neurotoxicity in Wistar rats

OBJECTIVE(S): Acrylamide (ACR) has broad applications in different industries. It also forms in food during heating process. Oxidative stress has a critical role in ACR-induced neurotoxicity in both in vitro and in vivo models; therefore, the aim of the current study was the evaluation of effects of...

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Autores principales: Mehri, Soghra, Shahi, Mehran, Razavi, Bibi Marjan, Hassani, Faezeh Vahdati, Hosseinzadeh, Hossein
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Mashhad University of Medical Sciences 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4387223/
https://www.ncbi.nlm.nih.gov/pubmed/25859305
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author Mehri, Soghra
Shahi, Mehran
Razavi, Bibi Marjan
Hassani, Faezeh Vahdati
Hosseinzadeh, Hossein
author_facet Mehri, Soghra
Shahi, Mehran
Razavi, Bibi Marjan
Hassani, Faezeh Vahdati
Hosseinzadeh, Hossein
author_sort Mehri, Soghra
collection PubMed
description OBJECTIVE(S): Acrylamide (ACR) has broad applications in different industries. It also forms in food during heating process. Oxidative stress has a critical role in ACR-induced neurotoxicity in both in vitro and in vivo models; therefore, the aim of the current study was the evaluation of effects of thymoquinone, the main constituent of volatile oil from Nigella sativa seeds in ACR-induced neurotoxicity. MATERIALS AND METHODS: Male Wistar rats were treated with ACR (50 mg/kg IP) alone or with thymoquinone (TQ) (2.5, 5, 10 mg/kg IP) for 11 days. Two protocols were used in this study, A: in this one TQ and ACR were used simultaneously, B: Administration of TQ was started 1 week before ACR treatment and continued during exposure to ACR. At the end of the treatment, behavioral index (gait score) was examined for rats. After that, rats were sacrificed and molondialdehyde (MDA) as a marker of lipid peroxidation and glutathione (GSH) content were determined in cerebral cortex. RESULTS: Exposure to ACR led to severe gait abnormalities and treatment with TQ significantly decreased abnormalities. Level of MDA was elevated in cerebral cortex after exposure to ACR while TQ treatment significantly and in a dose-dependent manner reduced lipid peroxidation. Results clearly showed that there is no significant difference between two protocols of administration of TQ. CONCLUSION: It suggests the neuroprotective effect of TQ in this model in part, may be because of due the antioxidant activity of this natural compound.
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spelling pubmed-43872232015-04-09 Neuroprotective effect of thymoquinone in acrylamide-induced neurotoxicity in Wistar rats Mehri, Soghra Shahi, Mehran Razavi, Bibi Marjan Hassani, Faezeh Vahdati Hosseinzadeh, Hossein Iran J Basic Med Sci Original Article OBJECTIVE(S): Acrylamide (ACR) has broad applications in different industries. It also forms in food during heating process. Oxidative stress has a critical role in ACR-induced neurotoxicity in both in vitro and in vivo models; therefore, the aim of the current study was the evaluation of effects of thymoquinone, the main constituent of volatile oil from Nigella sativa seeds in ACR-induced neurotoxicity. MATERIALS AND METHODS: Male Wistar rats were treated with ACR (50 mg/kg IP) alone or with thymoquinone (TQ) (2.5, 5, 10 mg/kg IP) for 11 days. Two protocols were used in this study, A: in this one TQ and ACR were used simultaneously, B: Administration of TQ was started 1 week before ACR treatment and continued during exposure to ACR. At the end of the treatment, behavioral index (gait score) was examined for rats. After that, rats were sacrificed and molondialdehyde (MDA) as a marker of lipid peroxidation and glutathione (GSH) content were determined in cerebral cortex. RESULTS: Exposure to ACR led to severe gait abnormalities and treatment with TQ significantly decreased abnormalities. Level of MDA was elevated in cerebral cortex after exposure to ACR while TQ treatment significantly and in a dose-dependent manner reduced lipid peroxidation. Results clearly showed that there is no significant difference between two protocols of administration of TQ. CONCLUSION: It suggests the neuroprotective effect of TQ in this model in part, may be because of due the antioxidant activity of this natural compound. Mashhad University of Medical Sciences 2014-12 /pmc/articles/PMC4387223/ /pubmed/25859305 Text en Copyright: © Iranian Journal of Basic Medical Sciences http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Mehri, Soghra
Shahi, Mehran
Razavi, Bibi Marjan
Hassani, Faezeh Vahdati
Hosseinzadeh, Hossein
Neuroprotective effect of thymoquinone in acrylamide-induced neurotoxicity in Wistar rats
title Neuroprotective effect of thymoquinone in acrylamide-induced neurotoxicity in Wistar rats
title_full Neuroprotective effect of thymoquinone in acrylamide-induced neurotoxicity in Wistar rats
title_fullStr Neuroprotective effect of thymoquinone in acrylamide-induced neurotoxicity in Wistar rats
title_full_unstemmed Neuroprotective effect of thymoquinone in acrylamide-induced neurotoxicity in Wistar rats
title_short Neuroprotective effect of thymoquinone in acrylamide-induced neurotoxicity in Wistar rats
title_sort neuroprotective effect of thymoquinone in acrylamide-induced neurotoxicity in wistar rats
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4387223/
https://www.ncbi.nlm.nih.gov/pubmed/25859305
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