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Sevoflurane protects rat mixed cerebrocortical neuronal-glial cell cultures against transient oxygen-glucose deprivation : Involvement of glutamate uptake and reactive oxygen species
The purpose of this study was to clarify the role of glutamate and reactive oxygen species in sevoflurane-mediated neuroprotection on an in vitro model of ischemia-reoxygenation. Mature mixed cerebrocortical neuronal-glial cell cultures, treated or not with increasing concentrations of sevoflurane,...
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| Published in: | Anesthesiology (Philadelphia) 2006-11, Vol.105 (5), p.990-998 |
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| creator | CANAS, Paula T VELLY, Lionel J LABRANDE, Christelle N GUILLET, Benjamin A SAUTOU-MIRANDA, Valérie MASMEJEAN, Frédérique M NIEOULLON, André L GOUIN, Francois M BRUDER, Nicolas J PISANO, Pascale S |
| description | The purpose of this study was to clarify the role of glutamate and reactive oxygen species in sevoflurane-mediated neuroprotection on an in vitro model of ischemia-reoxygenation.
Mature mixed cerebrocortical neuronal-glial cell cultures, treated or not with increasing concentrations of sevoflurane, were exposed to 90 min combined oxygen-glucose deprivation (OGD) in an anaerobic chamber followed by reoxygenation. Cell death was quantified by lactate dehydrogenase release into the media and cell viability by reduction of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium by mitochondrial succinate dehydrogenase. Extracellular concentrations of glutamate and glutamate uptake were assessed at the end of the ischemic injury by high-performance liquid chromatography and incorporation of L-[H]glutamate into cells, respectively. Free radical generation in cells was assessed 6 h after OGD during the reoxygenation period using 2',7'-dichlorofluorescin diacetate, which reacts with intracellular radicals to be converted to its fluorescent product, 2',7'-dichlorofluorescin, in cell cytosol.
Twenty-four hours after OGD, sevoflurane, in a concentration-dependent manner, significantly reduced lactate dehydrogenase release and increased cell viability. At the end of OGD, sevoflurane was able to reduce the OGD-induced decrease in glutamate uptake. This effect was impaired in the presence of threo-3-methyl glutamate, a specific inhibitor of the glial transporter GLT1. Sevoflurane counteracted the increase in extracellular level of glutamate during OGD and the generation of reactive oxygen species during reoxygenation.
Sevoflurane had a neuroprotective effect in this in vitro model of ischemia-reoxygenation. This beneficial effect may be explained, at least in part, by sevoflurane-induced antiexcitotoxic properties during OGD, probably depending on GLT1, and by sevoflurane-induced decrease of reactive oxygen species generation during reoxygenation. |
| doi_str_mv | 10.1097/00000542-200611000-00021 |
| format | article |
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Mature mixed cerebrocortical neuronal-glial cell cultures, treated or not with increasing concentrations of sevoflurane, were exposed to 90 min combined oxygen-glucose deprivation (OGD) in an anaerobic chamber followed by reoxygenation. Cell death was quantified by lactate dehydrogenase release into the media and cell viability by reduction of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium by mitochondrial succinate dehydrogenase. Extracellular concentrations of glutamate and glutamate uptake were assessed at the end of the ischemic injury by high-performance liquid chromatography and incorporation of L-[H]glutamate into cells, respectively. Free radical generation in cells was assessed 6 h after OGD during the reoxygenation period using 2',7'-dichlorofluorescin diacetate, which reacts with intracellular radicals to be converted to its fluorescent product, 2',7'-dichlorofluorescin, in cell cytosol.
Twenty-four hours after OGD, sevoflurane, in a concentration-dependent manner, significantly reduced lactate dehydrogenase release and increased cell viability. At the end of OGD, sevoflurane was able to reduce the OGD-induced decrease in glutamate uptake. This effect was impaired in the presence of threo-3-methyl glutamate, a specific inhibitor of the glial transporter GLT1. Sevoflurane counteracted the increase in extracellular level of glutamate during OGD and the generation of reactive oxygen species during reoxygenation.
Sevoflurane had a neuroprotective effect in this in vitro model of ischemia-reoxygenation. This beneficial effect may be explained, at least in part, by sevoflurane-induced antiexcitotoxic properties during OGD, probably depending on GLT1, and by sevoflurane-induced decrease of reactive oxygen species generation during reoxygenation.</description><identifier>ISSN: 0003-3022</identifier><identifier>EISSN: 1528-1175</identifier><identifier>DOI: 10.1097/00000542-200611000-00021</identifier><identifier>PMID: 17065894</identifier><identifier>CODEN: ANESAV</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott</publisher><subject>Anesthesia ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Biological and medical sciences ; Biological Transport, Active - drug effects ; Cell Hypoxia - drug effects ; Cells, Cultured ; Cellular Biology ; Cerebral Cortex - cytology ; Cerebral Cortex - drug effects ; Cerebral Cortex - metabolism ; Coculture Techniques ; Glucose - metabolism ; Glutamic Acid - metabolism ; Life Sciences ; Medical sciences ; Methyl Ethers - pharmacology ; Neuroglia - drug effects ; Neuroglia - metabolism ; Neurons - drug effects ; Neurons - metabolism ; Neuroprotective Agents - pharmacology ; Rats ; Reactive Oxygen Species - metabolism ; Sevoflurane</subject><ispartof>Anesthesiology (Philadelphia), 2006-11, Vol.105 (5), p.990-998</ispartof><rights>2006 INIST-CNRS</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><orcidid>0000-0002-3944-3752</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,786,790,891,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18245775$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17065894$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00306708$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>CANAS, Paula T</creatorcontrib><creatorcontrib>VELLY, Lionel J</creatorcontrib><creatorcontrib>LABRANDE, Christelle N</creatorcontrib><creatorcontrib>GUILLET, Benjamin A</creatorcontrib><creatorcontrib>SAUTOU-MIRANDA, Valérie</creatorcontrib><creatorcontrib>MASMEJEAN, Frédérique M</creatorcontrib><creatorcontrib>NIEOULLON, André L</creatorcontrib><creatorcontrib>GOUIN, Francois M</creatorcontrib><creatorcontrib>BRUDER, Nicolas J</creatorcontrib><creatorcontrib>PISANO, Pascale S</creatorcontrib><title>Sevoflurane protects rat mixed cerebrocortical neuronal-glial cell cultures against transient oxygen-glucose deprivation : Involvement of glutamate uptake and reactive oxygen species</title><title>Anesthesiology (Philadelphia)</title><addtitle>Anesthesiology</addtitle><description>The purpose of this study was to clarify the role of glutamate and reactive oxygen species in sevoflurane-mediated neuroprotection on an in vitro model of ischemia-reoxygenation.
Mature mixed cerebrocortical neuronal-glial cell cultures, treated or not with increasing concentrations of sevoflurane, were exposed to 90 min combined oxygen-glucose deprivation (OGD) in an anaerobic chamber followed by reoxygenation. Cell death was quantified by lactate dehydrogenase release into the media and cell viability by reduction of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium by mitochondrial succinate dehydrogenase. Extracellular concentrations of glutamate and glutamate uptake were assessed at the end of the ischemic injury by high-performance liquid chromatography and incorporation of L-[H]glutamate into cells, respectively. Free radical generation in cells was assessed 6 h after OGD during the reoxygenation period using 2',7'-dichlorofluorescin diacetate, which reacts with intracellular radicals to be converted to its fluorescent product, 2',7'-dichlorofluorescin, in cell cytosol.
Twenty-four hours after OGD, sevoflurane, in a concentration-dependent manner, significantly reduced lactate dehydrogenase release and increased cell viability. At the end of OGD, sevoflurane was able to reduce the OGD-induced decrease in glutamate uptake. This effect was impaired in the presence of threo-3-methyl glutamate, a specific inhibitor of the glial transporter GLT1. Sevoflurane counteracted the increase in extracellular level of glutamate during OGD and the generation of reactive oxygen species during reoxygenation.
Sevoflurane had a neuroprotective effect in this in vitro model of ischemia-reoxygenation. This beneficial effect may be explained, at least in part, by sevoflurane-induced antiexcitotoxic properties during OGD, probably depending on GLT1, and by sevoflurane-induced decrease of reactive oxygen species generation during reoxygenation.</description><subject>Anesthesia</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biological Transport, Active - drug effects</subject><subject>Cell Hypoxia - drug effects</subject><subject>Cells, Cultured</subject><subject>Cellular Biology</subject><subject>Cerebral Cortex - cytology</subject><subject>Cerebral Cortex - drug effects</subject><subject>Cerebral Cortex - metabolism</subject><subject>Coculture Techniques</subject><subject>Glucose - metabolism</subject><subject>Glutamic Acid - metabolism</subject><subject>Life Sciences</subject><subject>Medical sciences</subject><subject>Methyl Ethers - pharmacology</subject><subject>Neuroglia - drug effects</subject><subject>Neuroglia - metabolism</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Rats</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Sevoflurane</subject><issn>0003-3022</issn><issn>1528-1175</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNpFkdtu1DAQhi1ERbeFV0C-AYmLgA9JnHBXVfQgrcQFcB1NnMnWkMSLD1H7YjxfZ9sFLNnWjD79Gn3DGJfioxSt-SQOpypVoYSopaSioKvkC7aRlWoKKU31km2opwstlDplZzH-pNJUunnFTqURddW05Yb9-YarH6ccYEG-Dz6hTZEHSHx29zhwiwH74K0PyVmY-II5-AWmYjc5Ki1O9OQp5YCRww7cEhNPlBYdLon7-4cdLgRn6yPyAffBrZCcX_hnfrusflpxfgJHTlCCGRLyvE_wCzksAw8INrkVj0k87tE6jK_ZyQhTxDfH_5z9uPry_fKm2H69vr282BZ3yuhU2HLQAqVSo-6NbtVoe4BBq36wo-hLbZuxNUMrsK9EL5Ugk6BMI0bRDrUCo8_Zh-fcO5g6mn2G8NB5cN3NxbY79MiwqI1oVkns-2eWNP7OGFM3u3gQRGp9jl3dtG1J6yPw7RHM_YzDv9y_WyHg3RGASNJH0mld_M81qqwMrfIRipyibA</recordid><startdate>20061101</startdate><enddate>20061101</enddate><creator>CANAS, Paula T</creator><creator>VELLY, Lionel J</creator><creator>LABRANDE, Christelle N</creator><creator>GUILLET, Benjamin A</creator><creator>SAUTOU-MIRANDA, Valérie</creator><creator>MASMEJEAN, Frédérique M</creator><creator>NIEOULLON, André L</creator><creator>GOUIN, Francois M</creator><creator>BRUDER, Nicolas J</creator><creator>PISANO, Pascale S</creator><general>Lippincott</general><general>Lippincott, Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-3944-3752</orcidid></search><sort><creationdate>20061101</creationdate><title>Sevoflurane protects rat mixed cerebrocortical neuronal-glial cell cultures against transient oxygen-glucose deprivation : Involvement of glutamate uptake and reactive oxygen species</title><author>CANAS, Paula T ; VELLY, Lionel J ; LABRANDE, Christelle N ; GUILLET, Benjamin A ; SAUTOU-MIRANDA, Valérie ; MASMEJEAN, Frédérique M ; NIEOULLON, André L ; GOUIN, Francois M ; BRUDER, Nicolas J ; PISANO, Pascale S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h273t-c4d30e122f3b7392fcbaad32bdcf0b43c8f97d90eb50b120100a2780f09d62a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Anesthesia</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biological Transport, Active - drug effects</topic><topic>Cell Hypoxia - drug effects</topic><topic>Cells, Cultured</topic><topic>Cellular Biology</topic><topic>Cerebral Cortex - cytology</topic><topic>Cerebral Cortex - drug effects</topic><topic>Cerebral Cortex - metabolism</topic><topic>Coculture Techniques</topic><topic>Glucose - metabolism</topic><topic>Glutamic Acid - metabolism</topic><topic>Life Sciences</topic><topic>Medical sciences</topic><topic>Methyl Ethers - pharmacology</topic><topic>Neuroglia - drug effects</topic><topic>Neuroglia - metabolism</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Rats</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Sevoflurane</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CANAS, Paula T</creatorcontrib><creatorcontrib>VELLY, Lionel J</creatorcontrib><creatorcontrib>LABRANDE, Christelle N</creatorcontrib><creatorcontrib>GUILLET, Benjamin A</creatorcontrib><creatorcontrib>SAUTOU-MIRANDA, Valérie</creatorcontrib><creatorcontrib>MASMEJEAN, Frédérique M</creatorcontrib><creatorcontrib>NIEOULLON, André L</creatorcontrib><creatorcontrib>GOUIN, Francois M</creatorcontrib><creatorcontrib>BRUDER, Nicolas J</creatorcontrib><creatorcontrib>PISANO, Pascale S</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Anesthesiology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CANAS, Paula T</au><au>VELLY, Lionel J</au><au>LABRANDE, Christelle N</au><au>GUILLET, Benjamin A</au><au>SAUTOU-MIRANDA, Valérie</au><au>MASMEJEAN, Frédérique M</au><au>NIEOULLON, André L</au><au>GOUIN, Francois M</au><au>BRUDER, Nicolas J</au><au>PISANO, Pascale S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sevoflurane protects rat mixed cerebrocortical neuronal-glial cell cultures against transient oxygen-glucose deprivation : Involvement of glutamate uptake and reactive oxygen species</atitle><jtitle>Anesthesiology (Philadelphia)</jtitle><addtitle>Anesthesiology</addtitle><date>2006-11-01</date><risdate>2006</risdate><volume>105</volume><issue>5</issue><spage>990</spage><epage>998</epage><pages>990-998</pages><issn>0003-3022</issn><eissn>1528-1175</eissn><coden>ANESAV</coden><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>The purpose of this study was to clarify the role of glutamate and reactive oxygen species in sevoflurane-mediated neuroprotection on an in vitro model of ischemia-reoxygenation.
Mature mixed cerebrocortical neuronal-glial cell cultures, treated or not with increasing concentrations of sevoflurane, were exposed to 90 min combined oxygen-glucose deprivation (OGD) in an anaerobic chamber followed by reoxygenation. Cell death was quantified by lactate dehydrogenase release into the media and cell viability by reduction of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium by mitochondrial succinate dehydrogenase. Extracellular concentrations of glutamate and glutamate uptake were assessed at the end of the ischemic injury by high-performance liquid chromatography and incorporation of L-[H]glutamate into cells, respectively. Free radical generation in cells was assessed 6 h after OGD during the reoxygenation period using 2',7'-dichlorofluorescin diacetate, which reacts with intracellular radicals to be converted to its fluorescent product, 2',7'-dichlorofluorescin, in cell cytosol.
Twenty-four hours after OGD, sevoflurane, in a concentration-dependent manner, significantly reduced lactate dehydrogenase release and increased cell viability. At the end of OGD, sevoflurane was able to reduce the OGD-induced decrease in glutamate uptake. This effect was impaired in the presence of threo-3-methyl glutamate, a specific inhibitor of the glial transporter GLT1. Sevoflurane counteracted the increase in extracellular level of glutamate during OGD and the generation of reactive oxygen species during reoxygenation.
Sevoflurane had a neuroprotective effect in this in vitro model of ischemia-reoxygenation. This beneficial effect may be explained, at least in part, by sevoflurane-induced antiexcitotoxic properties during OGD, probably depending on GLT1, and by sevoflurane-induced decrease of reactive oxygen species generation during reoxygenation.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott</pub><pmid>17065894</pmid><doi>10.1097/00000542-200611000-00021</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-3944-3752</orcidid></addata></record> |
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| subjects | Anesthesia Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Biological and medical sciences Biological Transport, Active - drug effects Cell Hypoxia - drug effects Cells, Cultured Cellular Biology Cerebral Cortex - cytology Cerebral Cortex - drug effects Cerebral Cortex - metabolism Coculture Techniques Glucose - metabolism Glutamic Acid - metabolism Life Sciences Medical sciences Methyl Ethers - pharmacology Neuroglia - drug effects Neuroglia - metabolism Neurons - drug effects Neurons - metabolism Neuroprotective Agents - pharmacology Rats Reactive Oxygen Species - metabolism Sevoflurane |
| title | Sevoflurane protects rat mixed cerebrocortical neuronal-glial cell cultures against transient oxygen-glucose deprivation : Involvement of glutamate uptake and reactive oxygen species |
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