Post-Injury Administration of Tert-butylhydroquinone Attenuates Acute Neurological Injury After Intracerebral Hemorrhage in Mice
Intracerebral hemorrhage (ICH) is a severe form of stroke with substantial public health impact. Notably, there is no effective treatment for ICH. Given the role of transcription factor Nrf2 (NF-E2-related factor 2) in antioxidant signaling, herein, we tested the efficacy of tert-butylhydroquinone (...
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| Veröffentlicht in: | Journal of molecular neuroscience 2016-04, Vol.58 (4), p.525-531 |
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| creator | Sukumari-Ramesh, Sangeetha Alleyne, Cargill H. |
| description | Intracerebral hemorrhage (ICH) is a severe form of stroke with substantial public health impact. Notably, there is no effective treatment for ICH. Given the role of transcription factor Nrf2 (NF-E2-related factor 2) in antioxidant signaling, herein, we tested the efficacy of tert-butylhydroquinone (TBHQ), a selective inducer of Nrf2 in a preclinical model of ICH. Male CD1 mice were subjected to experimental intracerebral hemorrhage and administered intraperitoneally with TBHQ. The administration of TBHQ enhanced the DNA-binding activity of Nrf2 in the brain and reduced oxidative brain damage in comparison to vehicle-treated ICH. In addition, TBHQ treatment reduced microglial activation with concomitant reduction in the release of proinflammatory cytokine interleukin-1β (IL-1 β). Furthermore, TBHQ treatment attenuated neurodegeneration and improved neurological outcomes after ICH. Altogether, the data demonstrate the efficacy of post-injury administration of TBHQ in attenuating acute neurological injury after ICH. |
| doi_str_mv | 10.1007/s12031-016-0722-y |
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Notably, there is no effective treatment for ICH. Given the role of transcription factor Nrf2 (NF-E2-related factor 2) in antioxidant signaling, herein, we tested the efficacy of tert-butylhydroquinone (TBHQ), a selective inducer of Nrf2 in a preclinical model of ICH. Male CD1 mice were subjected to experimental intracerebral hemorrhage and administered intraperitoneally with TBHQ. The administration of TBHQ enhanced the DNA-binding activity of Nrf2 in the brain and reduced oxidative brain damage in comparison to vehicle-treated ICH. In addition, TBHQ treatment reduced microglial activation with concomitant reduction in the release of proinflammatory cytokine interleukin-1β (IL-1 β). Furthermore, TBHQ treatment attenuated neurodegeneration and improved neurological outcomes after ICH. Altogether, the data demonstrate the efficacy of post-injury administration of TBHQ in attenuating acute neurological injury after ICH.</description><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-016-0722-y</identifier><identifier>PMID: 26867538</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Antibodies ; Antioxidants ; Biomedical and Life Sciences ; Biomedicine ; Brain damage ; Cell Biology ; Cerebral Hemorrhage - drug therapy ; Hematoma ; Hemorrhage ; Hydroquinones - administration & dosage ; Hydroquinones - pharmacology ; Hydroquinones - therapeutic use ; Interleukins - metabolism ; Male ; Mice ; Microglia - drug effects ; Microglia - metabolism ; Neurochemistry ; Neurology ; Neuroprotective Agents - administration & dosage ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Neurosciences ; NF-E2-Related Factor 2 - metabolism ; Oxidation ; Oxidative stress ; Protein Binding ; Proteins ; Proteomics ; Stroke ; Transcription factors</subject><ispartof>Journal of molecular neuroscience, 2016-04, Vol.58 (4), p.525-531</ispartof><rights>Springer Science+Business Media New York 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-98e05b33efd50c547757dc24a476bbc1d4f575ee7756583291cb24fa1a606a463</citedby><cites>FETCH-LOGICAL-c471t-98e05b33efd50c547757dc24a476bbc1d4f575ee7756583291cb24fa1a606a463</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12031-016-0722-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12031-016-0722-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26867538$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sukumari-Ramesh, Sangeetha</creatorcontrib><creatorcontrib>Alleyne, Cargill H.</creatorcontrib><title>Post-Injury Administration of Tert-butylhydroquinone Attenuates Acute Neurological Injury After Intracerebral Hemorrhage in Mice</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>Intracerebral hemorrhage (ICH) is a severe form of stroke with substantial public health impact. Notably, there is no effective treatment for ICH. Given the role of transcription factor Nrf2 (NF-E2-related factor 2) in antioxidant signaling, herein, we tested the efficacy of tert-butylhydroquinone (TBHQ), a selective inducer of Nrf2 in a preclinical model of ICH. Male CD1 mice were subjected to experimental intracerebral hemorrhage and administered intraperitoneally with TBHQ. The administration of TBHQ enhanced the DNA-binding activity of Nrf2 in the brain and reduced oxidative brain damage in comparison to vehicle-treated ICH. In addition, TBHQ treatment reduced microglial activation with concomitant reduction in the release of proinflammatory cytokine interleukin-1β (IL-1 β). Furthermore, TBHQ treatment attenuated neurodegeneration and improved neurological outcomes after ICH. Altogether, the data demonstrate the efficacy of post-injury administration of TBHQ in attenuating acute neurological injury after ICH.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Antioxidants</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain damage</subject><subject>Cell Biology</subject><subject>Cerebral Hemorrhage - drug therapy</subject><subject>Hematoma</subject><subject>Hemorrhage</subject><subject>Hydroquinones - administration & dosage</subject><subject>Hydroquinones - pharmacology</subject><subject>Hydroquinones - therapeutic use</subject><subject>Interleukins - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Microglia - drug effects</subject><subject>Microglia - metabolism</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neuroprotective Agents - administration & dosage</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Neurosciences</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Oxidation</subject><subject>Oxidative stress</subject><subject>Protein Binding</subject><subject>Proteins</subject><subject>Proteomics</subject><subject>Stroke</subject><subject>Transcription factors</subject><issn>0895-8696</issn><issn>1559-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkUtv1TAQRi0EopfCD2CDIrFhY_A4fiTLq6rQSuWxKOvIcSa3uUrs4sciO346jm6LEBISq5Fnzhxr9BHyGth7YEx_iMBZDZSBokxzTtcnZAdSthRAqadkx5pW0ka16oy8iPHIGAcBzXNyxlWjtKybHfn5zcdEr90xh7XaD8vkppiCSZN3lR-rWwyJ9jmt8906BP8jT847rPYpocsmYaz2NiesvmAOfvaHyZq5erSNCUN5FJ3FgH0ooytcfAh35oDV5KrPk8WX5Nlo5oivHuo5-f7x8vbiit58_XR9sb-hVmhItG2Qyb6ucRwks1JoLfVguTBCq763MIhRaolY-ko2NW_B9lyMBoxiyghVn5N3J-_9dgbG1C1TtDjPxqHPsQPdSC55A-J_UABZC9isb_9Cjz4HVw7ZKCYkSMEKBSfKBh9jwLG7D9NiwtoB67Yku1OSXUmy25Ls1rLz5sGc-wWH3xuP0RWAn4BYRu6A4Y-v_2n9BQOUqnk</recordid><startdate>20160401</startdate><enddate>20160401</enddate><creator>Sukumari-Ramesh, Sangeetha</creator><creator>Alleyne, Cargill H.</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20160401</creationdate><title>Post-Injury Administration of Tert-butylhydroquinone Attenuates Acute Neurological Injury After Intracerebral Hemorrhage in Mice</title><author>Sukumari-Ramesh, Sangeetha ; Alleyne, Cargill H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-98e05b33efd50c547757dc24a476bbc1d4f575ee7756583291cb24fa1a606a463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Antioxidants</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain damage</topic><topic>Cell Biology</topic><topic>Cerebral Hemorrhage - drug therapy</topic><topic>Hematoma</topic><topic>Hemorrhage</topic><topic>Hydroquinones - administration & dosage</topic><topic>Hydroquinones - pharmacology</topic><topic>Hydroquinones - therapeutic use</topic><topic>Interleukins - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Microglia - drug effects</topic><topic>Microglia - metabolism</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neuroprotective Agents - administration & dosage</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Neurosciences</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Oxidation</topic><topic>Oxidative stress</topic><topic>Protein Binding</topic><topic>Proteins</topic><topic>Proteomics</topic><topic>Stroke</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sukumari-Ramesh, Sangeetha</creatorcontrib><creatorcontrib>Alleyne, Cargill H.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sukumari-Ramesh, Sangeetha</au><au>Alleyne, Cargill H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Post-Injury Administration of Tert-butylhydroquinone Attenuates Acute Neurological Injury After Intracerebral Hemorrhage in Mice</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2016-04-01</date><risdate>2016</risdate><volume>58</volume><issue>4</issue><spage>525</spage><epage>531</epage><pages>525-531</pages><issn>0895-8696</issn><eissn>1559-1166</eissn><abstract>Intracerebral hemorrhage (ICH) is a severe form of stroke with substantial public health impact. Notably, there is no effective treatment for ICH. Given the role of transcription factor Nrf2 (NF-E2-related factor 2) in antioxidant signaling, herein, we tested the efficacy of tert-butylhydroquinone (TBHQ), a selective inducer of Nrf2 in a preclinical model of ICH. Male CD1 mice were subjected to experimental intracerebral hemorrhage and administered intraperitoneally with TBHQ. The administration of TBHQ enhanced the DNA-binding activity of Nrf2 in the brain and reduced oxidative brain damage in comparison to vehicle-treated ICH. In addition, TBHQ treatment reduced microglial activation with concomitant reduction in the release of proinflammatory cytokine interleukin-1β (IL-1 β). Furthermore, TBHQ treatment attenuated neurodegeneration and improved neurological outcomes after ICH. Altogether, the data demonstrate the efficacy of post-injury administration of TBHQ in attenuating acute neurological injury after ICH.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>26867538</pmid><doi>10.1007/s12031-016-0722-y</doi><tpages>7</tpages></addata></record> |
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| subjects | Animals Antibodies Antioxidants Biomedical and Life Sciences Biomedicine Brain damage Cell Biology Cerebral Hemorrhage - drug therapy Hematoma Hemorrhage Hydroquinones - administration & dosage Hydroquinones - pharmacology Hydroquinones - therapeutic use Interleukins - metabolism Male Mice Microglia - drug effects Microglia - metabolism Neurochemistry Neurology Neuroprotective Agents - administration & dosage Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Neurosciences NF-E2-Related Factor 2 - metabolism Oxidation Oxidative stress Protein Binding Proteins Proteomics Stroke Transcription factors |
| title | Post-Injury Administration of Tert-butylhydroquinone Attenuates Acute Neurological Injury After Intracerebral Hemorrhage in Mice |
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