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Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF-κB, ICAM-1, MMP-9 and caspase-3 expression

Reperfusion is the only approved therapy for acute ischemic stroke; however, it can cause excessive inflammation responses and aggravate brain damage. Therefore, supplementary treatment against inflammation caused by reperfusion is required. In a previous study from our group, curcumin was demonstra...

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Autores principales: Li, Wei, Suwanwela, Nijasri Charnnarong, Patumraj, Suthiluk
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647023/
https://www.ncbi.nlm.nih.gov/pubmed/28849007
http://dx.doi.org/10.3892/mmr.2017.7205
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author Li, Wei
Suwanwela, Nijasri Charnnarong
Patumraj, Suthiluk
author_facet Li, Wei
Suwanwela, Nijasri Charnnarong
Patumraj, Suthiluk
author_sort Li, Wei
collection PubMed
description Reperfusion is the only approved therapy for acute ischemic stroke; however, it can cause excessive inflammation responses and aggravate brain damage. Therefore, supplementary treatment against inflammation caused by reperfusion is required. In a previous study from our group, curcumin was demonstrated to decrease infarction volume, brain edema and blood-brain barrier (BBB) disruption against cerebral ischemia/reperfusion (I/R) injury. However, the underlying mechanisms remain unclear. The present study was conducted to understand whether curcumin protects against cerebral I/R injury through anti-inflammatory and antiapoptotic properties. Ischemia for 1 h was induced in vivo in Wistar rats by middle cerebral artery occlusion (MCAO), followed by reperfusion for 24 h, and curcumin was injected intraperitoneally at 30 min prior to reperfusion. Immunohistochemistry was performed to analyze the expression levels of nuclear factor (NF)-κB, intercellular adhesion molecule (ICAM)-1, matrix metalloproteinase (MMP)-9 and caspase-3. The findings revealed that inflammation (NF-κB, ICAM-1 and MMP-9) and apoptosis (caspase-3)-related markers were significantly downregulated in the curcumin-treated MCAO group compared with the vehicle-treated MCAO group. Furthermore, brain infarction size, brain edema and neurological dysfunction were attenuated in the curcumin-treated MCAO group compared with the vehicle-treated MCAO group. Taken together, the present results provided evidence that the protective effect of curcumin against cerebral I/R injury might be mediated by anti-inflammatory and anti-apoptotic properties. Therefore, curcumin may be a promising supplementary agent against cerebral I/R injury in the future.
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spelling pubmed-56470232017-10-24 Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF-κB, ICAM-1, MMP-9 and caspase-3 expression Li, Wei Suwanwela, Nijasri Charnnarong Patumraj, Suthiluk Mol Med Rep Articles Reperfusion is the only approved therapy for acute ischemic stroke; however, it can cause excessive inflammation responses and aggravate brain damage. Therefore, supplementary treatment against inflammation caused by reperfusion is required. In a previous study from our group, curcumin was demonstrated to decrease infarction volume, brain edema and blood-brain barrier (BBB) disruption against cerebral ischemia/reperfusion (I/R) injury. However, the underlying mechanisms remain unclear. The present study was conducted to understand whether curcumin protects against cerebral I/R injury through anti-inflammatory and antiapoptotic properties. Ischemia for 1 h was induced in vivo in Wistar rats by middle cerebral artery occlusion (MCAO), followed by reperfusion for 24 h, and curcumin was injected intraperitoneally at 30 min prior to reperfusion. Immunohistochemistry was performed to analyze the expression levels of nuclear factor (NF)-κB, intercellular adhesion molecule (ICAM)-1, matrix metalloproteinase (MMP)-9 and caspase-3. The findings revealed that inflammation (NF-κB, ICAM-1 and MMP-9) and apoptosis (caspase-3)-related markers were significantly downregulated in the curcumin-treated MCAO group compared with the vehicle-treated MCAO group. Furthermore, brain infarction size, brain edema and neurological dysfunction were attenuated in the curcumin-treated MCAO group compared with the vehicle-treated MCAO group. Taken together, the present results provided evidence that the protective effect of curcumin against cerebral I/R injury might be mediated by anti-inflammatory and anti-apoptotic properties. Therefore, curcumin may be a promising supplementary agent against cerebral I/R injury in the future. D.A. Spandidos 2017-10 2017-08-10 /pmc/articles/PMC5647023/ /pubmed/28849007 http://dx.doi.org/10.3892/mmr.2017.7205 Text en Copyright: © Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Li, Wei
Suwanwela, Nijasri Charnnarong
Patumraj, Suthiluk
Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF-κB, ICAM-1, MMP-9 and caspase-3 expression
title Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF-κB, ICAM-1, MMP-9 and caspase-3 expression
title_full Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF-κB, ICAM-1, MMP-9 and caspase-3 expression
title_fullStr Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF-κB, ICAM-1, MMP-9 and caspase-3 expression
title_full_unstemmed Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF-κB, ICAM-1, MMP-9 and caspase-3 expression
title_short Curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of NF-κB, ICAM-1, MMP-9 and caspase-3 expression
title_sort curcumin prevents reperfusion injury following ischemic stroke in rats via inhibition of nf-κb, icam-1, mmp-9 and caspase-3 expression
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647023/
https://www.ncbi.nlm.nih.gov/pubmed/28849007
http://dx.doi.org/10.3892/mmr.2017.7205
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