Involvement of IL-17 in Secondary Brain Injury After a Traumatic Brain Injury in Rats
The pro-inflammatory activity of interleukin 17, which is produced by the IL-23/IL-17 axis, has been associated with the pathogenesis of traumatic brain injury (TBI). The study investigated the potential role of IL-17 in secondary brain injury of TBI in a rat model. Our data showed that the levels o...
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| Veröffentlicht in: | Neuromolecular medicine 2017-12, Vol.19 (4), p.541-554 |
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| creator | Li, Tan Zhang, Yong-mei Han, Dong Hua, Rong Guo, Bing-nan Hu, Shu-qun Yan, Xian-liang Xu, Tie |
| description | The pro-inflammatory activity of interleukin 17, which is produced by the IL-23/IL-17 axis, has been associated with the pathogenesis of traumatic brain injury (TBI). The study investigated the potential role of IL-17 in secondary brain injury of TBI in a rat model. Our data showed that the levels of IL-17 increased from 6 h to 7 days and peaked at 3 days, in both the CNS and serum, which were consistent with the severity of secondary brain injury. The IL-23 inhibitor suberoylanilide hydroxamic acid (SAHA) treatment markedly decreased the expressions of IL-17 and apoptosis-associated proteins cleaved caspase-3 and increased the protein ratio of Bcl-2 (B cell lymphoma/leukemia-2)/Bax (Bcl-2-associated X protein). Meanwhile, neuronal apoptosis was reduced, and neural function was improved after SAHA treatment. This study suggests that IL-17 is involved in secondary brain injury after TBI. Administering an IL-23 inhibitor and thereby blocking the IL-23/IL-17 axis may be beneficial in the treatment of TBI. |
| doi_str_mv | 10.1007/s12017-017-8468-4 |
| format | Article |
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The study investigated the potential role of IL-17 in secondary brain injury of TBI in a rat model. Our data showed that the levels of IL-17 increased from 6 h to 7 days and peaked at 3 days, in both the CNS and serum, which were consistent with the severity of secondary brain injury. The IL-23 inhibitor suberoylanilide hydroxamic acid (SAHA) treatment markedly decreased the expressions of IL-17 and apoptosis-associated proteins cleaved caspase-3 and increased the protein ratio of Bcl-2 (B cell lymphoma/leukemia-2)/Bax (Bcl-2-associated X protein). Meanwhile, neuronal apoptosis was reduced, and neural function was improved after SAHA treatment. This study suggests that IL-17 is involved in secondary brain injury after TBI. Administering an IL-23 inhibitor and thereby blocking the IL-23/IL-17 axis may be beneficial in the treatment of TBI.</description><identifier>ISSN: 1535-1084</identifier><identifier>EISSN: 1559-1174</identifier><identifier>DOI: 10.1007/s12017-017-8468-4</identifier><identifier>PMID: 28916896</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Apoptosis ; Apoptosis - drug effects ; Apoptosis Regulatory Proteins - biosynthesis ; Apoptosis Regulatory Proteins - genetics ; BAX protein ; Bcl-2 protein ; Bcl-x protein ; Biomedical and Life Sciences ; Biomedicine ; Brain Damage, Chronic - etiology ; Brain Damage, Chronic - metabolism ; Brain Damage, Chronic - physiopathology ; Brain Damage, Chronic - prevention & control ; Brain Injuries, Traumatic - complications ; Brain Injuries, Traumatic - drug therapy ; Brain Injuries, Traumatic - metabolism ; Brain Injuries, Traumatic - physiopathology ; Caspase ; Caspase-3 ; Central nervous system ; Down-Regulation - drug effects ; Hydroxamic acid ; Hydroxamic Acids - pharmacology ; Hydroxamic Acids - therapeutic use ; Inflammation ; Interleukin 17 ; Interleukin 23 ; Interleukin-17 - blood ; Interleukin-17 - cerebrospinal fluid ; Interleukin-17 - genetics ; Interleukin-17 - physiology ; Interleukin-23 - antagonists & inhibitors ; Interleukin-23 - physiology ; Internal Medicine ; Lymphocytes B ; Lymphoma ; Male ; Nerve Tissue Proteins - biosynthesis ; Nerve Tissue Proteins - blood ; Nerve Tissue Proteins - cerebrospinal fluid ; Nerve Tissue Proteins - genetics ; Neurology ; Neurons - pathology ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; Neurosciences ; Original Paper ; Rats ; Rats, Sprague-Dawley ; Rodents ; Time Factors ; Traumatic brain injury ; Vorinostat</subject><ispartof>Neuromolecular medicine, 2017-12, Vol.19 (4), p.541-554</ispartof><rights>Springer Science+Business Media, LLC 2017</rights><rights>NeuroMolecular Medicine is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-de7fe67c42b84ebfc17cbb4c52d5a26ae8fbbbf5af2c4f818ff6a6c945cda77a3</citedby><cites>FETCH-LOGICAL-c438t-de7fe67c42b84ebfc17cbb4c52d5a26ae8fbbbf5af2c4f818ff6a6c945cda77a3</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/s12017-017-8468-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12017-017-8468-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28916896$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Tan</creatorcontrib><creatorcontrib>Zhang, Yong-mei</creatorcontrib><creatorcontrib>Han, Dong</creatorcontrib><creatorcontrib>Hua, Rong</creatorcontrib><creatorcontrib>Guo, Bing-nan</creatorcontrib><creatorcontrib>Hu, Shu-qun</creatorcontrib><creatorcontrib>Yan, Xian-liang</creatorcontrib><creatorcontrib>Xu, Tie</creatorcontrib><title>Involvement of IL-17 in Secondary Brain Injury After a Traumatic Brain Injury in Rats</title><title>Neuromolecular medicine</title><addtitle>Neuromol Med</addtitle><addtitle>Neuromolecular Med</addtitle><description>The pro-inflammatory activity of interleukin 17, which is produced by the IL-23/IL-17 axis, has been associated with the pathogenesis of traumatic brain injury (TBI). The study investigated the potential role of IL-17 in secondary brain injury of TBI in a rat model. Our data showed that the levels of IL-17 increased from 6 h to 7 days and peaked at 3 days, in both the CNS and serum, which were consistent with the severity of secondary brain injury. The IL-23 inhibitor suberoylanilide hydroxamic acid (SAHA) treatment markedly decreased the expressions of IL-17 and apoptosis-associated proteins cleaved caspase-3 and increased the protein ratio of Bcl-2 (B cell lymphoma/leukemia-2)/Bax (Bcl-2-associated X protein). Meanwhile, neuronal apoptosis was reduced, and neural function was improved after SAHA treatment. This study suggests that IL-17 is involved in secondary brain injury after TBI. Administering an IL-23 inhibitor and thereby blocking the IL-23/IL-17 axis may be beneficial in the treatment of TBI.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis Regulatory Proteins - biosynthesis</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>BAX protein</subject><subject>Bcl-2 protein</subject><subject>Bcl-x protein</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain Damage, Chronic - etiology</subject><subject>Brain Damage, Chronic - metabolism</subject><subject>Brain Damage, Chronic - physiopathology</subject><subject>Brain Damage, Chronic - prevention & control</subject><subject>Brain Injuries, Traumatic - complications</subject><subject>Brain Injuries, Traumatic - drug therapy</subject><subject>Brain Injuries, Traumatic - metabolism</subject><subject>Brain Injuries, Traumatic - physiopathology</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Central nervous system</subject><subject>Down-Regulation - drug effects</subject><subject>Hydroxamic acid</subject><subject>Hydroxamic Acids - pharmacology</subject><subject>Hydroxamic Acids - therapeutic use</subject><subject>Inflammation</subject><subject>Interleukin 17</subject><subject>Interleukin 23</subject><subject>Interleukin-17 - blood</subject><subject>Interleukin-17 - cerebrospinal fluid</subject><subject>Interleukin-17 - genetics</subject><subject>Interleukin-17 - physiology</subject><subject>Interleukin-23 - antagonists & inhibitors</subject><subject>Interleukin-23 - physiology</subject><subject>Internal Medicine</subject><subject>Lymphocytes B</subject><subject>Lymphoma</subject><subject>Male</subject><subject>Nerve Tissue Proteins - biosynthesis</subject><subject>Nerve Tissue Proteins - blood</subject><subject>Nerve Tissue Proteins - cerebrospinal fluid</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Neurology</subject><subject>Neurons - pathology</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Time Factors</subject><subject>Traumatic brain injury</subject><subject>Vorinostat</subject><issn>1535-1084</issn><issn>1559-1174</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</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>eNp1kEtLxDAQgIMorq7-AC9S8OKlmknz6nFdfBQWBN09lzRNpMu2XZN2wX9vSldRwcOQGeabmfAhdAH4BjAWtx4IBhEPISmXMT1AJ8BYGgMIejjkCYsBSzpBp96vMSYEAI7RhMgUuEz5CVplza7d7Extmi5qbZQtYhBR1USvRrdNqdxHdOdUqLNm3YdiZjvjIhUtnepr1VX6dztkL6rzZ-jIqo035_t3ilYP98v5U7x4fszms0WsaSK7uDTCGi40JYWkprAahC4KqhkpmSJcGWmLorBMWaKplSCt5YrrlDJdKiFUMkXX496ta99747u8rrw2m41qTNv7HFKKMSOEpQG9-oOu29414XeB4sFXIoAHCkZKu9Z7Z2y-dVUdLOSA88F5PjrPhxic5zTMXO4390Vtyu-JL8kBICPgQ6t5M-7H6X-3fgJQ34vU</recordid><startdate>20171201</startdate><enddate>20171201</enddate><creator>Li, Tan</creator><creator>Zhang, Yong-mei</creator><creator>Han, Dong</creator><creator>Hua, Rong</creator><creator>Guo, Bing-nan</creator><creator>Hu, Shu-qun</creator><creator>Yan, Xian-liang</creator><creator>Xu, Tie</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>7QP</scope><scope>7QR</scope><scope>7TK</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>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</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>20171201</creationdate><title>Involvement of IL-17 in Secondary Brain Injury After a Traumatic Brain Injury in Rats</title><author>Li, Tan ; Zhang, Yong-mei ; Han, Dong ; Hua, Rong ; Guo, Bing-nan ; Hu, Shu-qun ; Yan, Xian-liang ; Xu, Tie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-de7fe67c42b84ebfc17cbb4c52d5a26ae8fbbbf5af2c4f818ff6a6c945cda77a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis Regulatory Proteins - biosynthesis</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>BAX protein</topic><topic>Bcl-2 protein</topic><topic>Bcl-x protein</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain Damage, Chronic - etiology</topic><topic>Brain Damage, Chronic - metabolism</topic><topic>Brain Damage, Chronic - physiopathology</topic><topic>Brain Damage, Chronic - prevention & control</topic><topic>Brain Injuries, Traumatic - complications</topic><topic>Brain Injuries, Traumatic - drug therapy</topic><topic>Brain Injuries, Traumatic - metabolism</topic><topic>Brain Injuries, Traumatic - physiopathology</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Central nervous system</topic><topic>Down-Regulation - drug effects</topic><topic>Hydroxamic acid</topic><topic>Hydroxamic Acids - pharmacology</topic><topic>Hydroxamic Acids - therapeutic use</topic><topic>Inflammation</topic><topic>Interleukin 17</topic><topic>Interleukin 23</topic><topic>Interleukin-17 - blood</topic><topic>Interleukin-17 - cerebrospinal fluid</topic><topic>Interleukin-17 - genetics</topic><topic>Interleukin-17 - physiology</topic><topic>Interleukin-23 - antagonists & inhibitors</topic><topic>Interleukin-23 - physiology</topic><topic>Internal Medicine</topic><topic>Lymphocytes B</topic><topic>Lymphoma</topic><topic>Male</topic><topic>Nerve Tissue Proteins - biosynthesis</topic><topic>Nerve Tissue Proteins - blood</topic><topic>Nerve Tissue Proteins - cerebrospinal fluid</topic><topic>Nerve Tissue Proteins - genetics</topic><topic>Neurology</topic><topic>Neurons - pathology</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Time Factors</topic><topic>Traumatic brain injury</topic><topic>Vorinostat</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Tan</creatorcontrib><creatorcontrib>Zhang, Yong-mei</creatorcontrib><creatorcontrib>Han, Dong</creatorcontrib><creatorcontrib>Hua, Rong</creatorcontrib><creatorcontrib>Guo, Bing-nan</creatorcontrib><creatorcontrib>Hu, Shu-qun</creatorcontrib><creatorcontrib>Yan, Xian-liang</creatorcontrib><creatorcontrib>Xu, Tie</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>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences 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>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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</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>Neuromolecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Tan</au><au>Zhang, Yong-mei</au><au>Han, Dong</au><au>Hua, Rong</au><au>Guo, Bing-nan</au><au>Hu, Shu-qun</au><au>Yan, Xian-liang</au><au>Xu, Tie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Involvement of IL-17 in Secondary Brain Injury After a Traumatic Brain Injury in Rats</atitle><jtitle>Neuromolecular medicine</jtitle><stitle>Neuromol Med</stitle><addtitle>Neuromolecular Med</addtitle><date>2017-12-01</date><risdate>2017</risdate><volume>19</volume><issue>4</issue><spage>541</spage><epage>554</epage><pages>541-554</pages><issn>1535-1084</issn><eissn>1559-1174</eissn><abstract>The pro-inflammatory activity of interleukin 17, which is produced by the IL-23/IL-17 axis, has been associated with the pathogenesis of traumatic brain injury (TBI). The study investigated the potential role of IL-17 in secondary brain injury of TBI in a rat model. Our data showed that the levels of IL-17 increased from 6 h to 7 days and peaked at 3 days, in both the CNS and serum, which were consistent with the severity of secondary brain injury. The IL-23 inhibitor suberoylanilide hydroxamic acid (SAHA) treatment markedly decreased the expressions of IL-17 and apoptosis-associated proteins cleaved caspase-3 and increased the protein ratio of Bcl-2 (B cell lymphoma/leukemia-2)/Bax (Bcl-2-associated X protein). Meanwhile, neuronal apoptosis was reduced, and neural function was improved after SAHA treatment. This study suggests that IL-17 is involved in secondary brain injury after TBI. Administering an IL-23 inhibitor and thereby blocking the IL-23/IL-17 axis may be beneficial in the treatment of TBI.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>28916896</pmid><doi>10.1007/s12017-017-8468-4</doi><tpages>14</tpages></addata></record> |
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| subjects | Animals Apoptosis Apoptosis - drug effects Apoptosis Regulatory Proteins - biosynthesis Apoptosis Regulatory Proteins - genetics BAX protein Bcl-2 protein Bcl-x protein Biomedical and Life Sciences Biomedicine Brain Damage, Chronic - etiology Brain Damage, Chronic - metabolism Brain Damage, Chronic - physiopathology Brain Damage, Chronic - prevention & control Brain Injuries, Traumatic - complications Brain Injuries, Traumatic - drug therapy Brain Injuries, Traumatic - metabolism Brain Injuries, Traumatic - physiopathology Caspase Caspase-3 Central nervous system Down-Regulation - drug effects Hydroxamic acid Hydroxamic Acids - pharmacology Hydroxamic Acids - therapeutic use Inflammation Interleukin 17 Interleukin 23 Interleukin-17 - blood Interleukin-17 - cerebrospinal fluid Interleukin-17 - genetics Interleukin-17 - physiology Interleukin-23 - antagonists & inhibitors Interleukin-23 - physiology Internal Medicine Lymphocytes B Lymphoma Male Nerve Tissue Proteins - biosynthesis Nerve Tissue Proteins - blood Nerve Tissue Proteins - cerebrospinal fluid Nerve Tissue Proteins - genetics Neurology Neurons - pathology Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use Neurosciences Original Paper Rats Rats, Sprague-Dawley Rodents Time Factors Traumatic brain injury Vorinostat |
| title | Involvement of IL-17 in Secondary Brain Injury After a Traumatic Brain Injury in Rats |
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