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Neuroprotective properties of Melissa officinalis after hypoxic-ischemic injury both in vitro and in vivo

BACKGROUND: Brain ischemia initiates several metabolic events leading to neuronal death. These events mediate large amount of damage that arises after some neurodegenerative disorders as well as transient brain ischemia. Melissa officinalis is considered as a helpful herbal plant in the prevention o...

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Autores principales: Bayat, Mohammad, Azami Tameh, Abolfazl, Hossein Ghahremani, Mohammad, Akbari, Mohammad, Mehr, Shahram Ejtemaei, Khanavi, Mahnaz, Hassanzadeh, Gholamreza
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3555743/
https://www.ncbi.nlm.nih.gov/pubmed/23351182
http://dx.doi.org/10.1186/2008-2231-20-42
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author Bayat, Mohammad
Azami Tameh, Abolfazl
Hossein Ghahremani, Mohammad
Akbari, Mohammad
Mehr, Shahram Ejtemaei
Khanavi, Mahnaz
Hassanzadeh, Gholamreza
author_facet Bayat, Mohammad
Azami Tameh, Abolfazl
Hossein Ghahremani, Mohammad
Akbari, Mohammad
Mehr, Shahram Ejtemaei
Khanavi, Mahnaz
Hassanzadeh, Gholamreza
author_sort Bayat, Mohammad
collection PubMed
description BACKGROUND: Brain ischemia initiates several metabolic events leading to neuronal death. These events mediate large amount of damage that arises after some neurodegenerative disorders as well as transient brain ischemia. Melissa officinalis is considered as a helpful herbal plant in the prevention of various neurological diseases like Alzheimer that is related with oxidative stress. METHODS: We examined the effect of Melissa officinalis on hypoxia induced neuronal death in a cortical neuronal culture system as in vitro model and transient hippocampal ischemia as in vivo model. Transient hippocampal ischemia was induced in male rats by tow vessel-occlusion for 20 min. After reperfusion, the histopathological changes and the levels inflammation, oxidative stress status, and caspase-3 activity in hippocampus were measured. RESULTS: Cytotoxicity assays showed a significant protection of a 10 μg/ml dose of Melissa against hypoxia in cultured neurons which was confirmed by a conventional staining (P<0.05). Melissa treatment decrease caspase3 activity (P<0.05) and TUNEL-positive cells significantly (P<0.01). Melissa oil has also inhibited malon dialdehyde level and attenuated decrease of Antioxidant Capacity in the hippocampus. Pro-inflammatory cytokines TNF-α, IL-1β and HIF-1α mRNA levels were highly increased after ischemia and treatment with Melissa significantly suppressed HIF-1α gene expression (P<0.05). DISCUSSION: Results showed that Melissa officinalis could be considered as a protective agent in various neurological diseases associated with ischemic brain injury.
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spelling pubmed-35557432013-01-31 Neuroprotective properties of Melissa officinalis after hypoxic-ischemic injury both in vitro and in vivo Bayat, Mohammad Azami Tameh, Abolfazl Hossein Ghahremani, Mohammad Akbari, Mohammad Mehr, Shahram Ejtemaei Khanavi, Mahnaz Hassanzadeh, Gholamreza Daru Research Article BACKGROUND: Brain ischemia initiates several metabolic events leading to neuronal death. These events mediate large amount of damage that arises after some neurodegenerative disorders as well as transient brain ischemia. Melissa officinalis is considered as a helpful herbal plant in the prevention of various neurological diseases like Alzheimer that is related with oxidative stress. METHODS: We examined the effect of Melissa officinalis on hypoxia induced neuronal death in a cortical neuronal culture system as in vitro model and transient hippocampal ischemia as in vivo model. Transient hippocampal ischemia was induced in male rats by tow vessel-occlusion for 20 min. After reperfusion, the histopathological changes and the levels inflammation, oxidative stress status, and caspase-3 activity in hippocampus were measured. RESULTS: Cytotoxicity assays showed a significant protection of a 10 μg/ml dose of Melissa against hypoxia in cultured neurons which was confirmed by a conventional staining (P<0.05). Melissa treatment decrease caspase3 activity (P<0.05) and TUNEL-positive cells significantly (P<0.01). Melissa oil has also inhibited malon dialdehyde level and attenuated decrease of Antioxidant Capacity in the hippocampus. Pro-inflammatory cytokines TNF-α, IL-1β and HIF-1α mRNA levels were highly increased after ischemia and treatment with Melissa significantly suppressed HIF-1α gene expression (P<0.05). DISCUSSION: Results showed that Melissa officinalis could be considered as a protective agent in various neurological diseases associated with ischemic brain injury. BioMed Central 2012-10-03 /pmc/articles/PMC3555743/ /pubmed/23351182 http://dx.doi.org/10.1186/2008-2231-20-42 Text en Copyright ©2012 Bayat et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Bayat, Mohammad
Azami Tameh, Abolfazl
Hossein Ghahremani, Mohammad
Akbari, Mohammad
Mehr, Shahram Ejtemaei
Khanavi, Mahnaz
Hassanzadeh, Gholamreza
Neuroprotective properties of Melissa officinalis after hypoxic-ischemic injury both in vitro and in vivo
title Neuroprotective properties of Melissa officinalis after hypoxic-ischemic injury both in vitro and in vivo
title_full Neuroprotective properties of Melissa officinalis after hypoxic-ischemic injury both in vitro and in vivo
title_fullStr Neuroprotective properties of Melissa officinalis after hypoxic-ischemic injury both in vitro and in vivo
title_full_unstemmed Neuroprotective properties of Melissa officinalis after hypoxic-ischemic injury both in vitro and in vivo
title_short Neuroprotective properties of Melissa officinalis after hypoxic-ischemic injury both in vitro and in vivo
title_sort neuroprotective properties of melissa officinalis after hypoxic-ischemic injury both in vitro and in vivo
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3555743/
https://www.ncbi.nlm.nih.gov/pubmed/23351182
http://dx.doi.org/10.1186/2008-2231-20-42
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