Sevoflurane Preconditioning Induces Neuroprotection Through Reactive Oxygen Species-Mediated Up-Regulation of Antioxidant Enzymes in Rats
It has been reported that sevoflurane preconditioning can induce neuroprotection, the mechanisms of which, however, are poorly elucidated. We designed the present study to examine the hypothesis that sevoflurane preconditioning could reduce cerebral ischemia- reperfusion injury through up-regulating...
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| Veröffentlicht in: | Anesthesia and analgesia 2011-04, Vol.112 (4), p.931-937 |
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| creator | Yang, Qianzi Dong, Hui Deng, Jiao Wang, Qiang Ye, Ruidong Li, Xuying Hu, Sheng Dong, Hailong Xiong, Lize |
| description | It has been reported that sevoflurane preconditioning can induce neuroprotection, the mechanisms of which, however, are poorly elucidated. We designed the present study to examine the hypothesis that sevoflurane preconditioning could reduce cerebral ischemia- reperfusion injury through up-regulating antioxidant enzyme activities before ischemic injury by generating reactive oxygen species (ROS).
In preconditioning groups, adult male Sprague-Dawley rats were pretreated with 1 hour sevoflurane exposure at a dose of 1%, 2%, or 4% for 5 consecutive days. At 24 hours after the last exposure, all rats were subjected to focal brain ischemia induced by middle cerebral artery occlusion for 120 minutes followed by 72-hour reperfusion. The role of ROS in ischemic tolerance was assessed by administration of the free radical scavenger dimethylthiourea and antioxidant N-acetylcysteine before each preconditioning. Brain ischemic injury was evaluated by neurologic behavior scores and brain infarct volume calculation. Antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase [GSH-px]) of brain tissue and blood serum were tested at 24 hours after the last sevoflurane preconditioning.
Sevoflurane preconditioning reduced infarct size and improved neurobehavioral outcome in a dose-dependent manner. The neuroprotective effects of sevoflurane preconditioning were abolished by dimethylthiourea and N-acetylcysteine. The activities of catalase and glutathione peroxidase (GSH-px) in the brain tissue were elevated by sevoflurane preconditioning before ischemic injury. The up-regulated activity of GSH-px in serum negatively correlated with brain infarct volume percentage.
Sevoflurane preconditioning induces cerebral ischemic tolerance in a dose- response manner through ROS release and consequent up-regulation of antioxidant enzyme activity before ischemic injury in rats. Serum GSH-px activity could be developed as a marker to assess the effectiveness of sevoflurane preconditioning before ischemia. |
| doi_str_mv | 10.1213/ANE.0b013e31820bcfa4 |
| format | Article |
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In preconditioning groups, adult male Sprague-Dawley rats were pretreated with 1 hour sevoflurane exposure at a dose of 1%, 2%, or 4% for 5 consecutive days. At 24 hours after the last exposure, all rats were subjected to focal brain ischemia induced by middle cerebral artery occlusion for 120 minutes followed by 72-hour reperfusion. The role of ROS in ischemic tolerance was assessed by administration of the free radical scavenger dimethylthiourea and antioxidant N-acetylcysteine before each preconditioning. Brain ischemic injury was evaluated by neurologic behavior scores and brain infarct volume calculation. Antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase [GSH-px]) of brain tissue and blood serum were tested at 24 hours after the last sevoflurane preconditioning.
Sevoflurane preconditioning reduced infarct size and improved neurobehavioral outcome in a dose-dependent manner. The neuroprotective effects of sevoflurane preconditioning were abolished by dimethylthiourea and N-acetylcysteine. The activities of catalase and glutathione peroxidase (GSH-px) in the brain tissue were elevated by sevoflurane preconditioning before ischemic injury. The up-regulated activity of GSH-px in serum negatively correlated with brain infarct volume percentage.
Sevoflurane preconditioning induces cerebral ischemic tolerance in a dose- response manner through ROS release and consequent up-regulation of antioxidant enzyme activity before ischemic injury in rats. Serum GSH-px activity could be developed as a marker to assess the effectiveness of sevoflurane preconditioning before ischemia.</description><identifier>ISSN: 0003-2999</identifier><identifier>EISSN: 1526-7598</identifier><identifier>DOI: 10.1213/ANE.0b013e31820bcfa4</identifier><identifier>PMID: 21385986</identifier><identifier>CODEN: AACRAT</identifier><language>eng</language><publisher>Hagerstown, MD: International Anesthesia Research Society</publisher><subject>Anesthesia ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Antioxidants - metabolism ; Biological and medical sciences ; Brain Ischemia - enzymology ; Brain Ischemia - prevention & control ; Cerebrovascular Circulation - drug effects ; Cerebrovascular Circulation - physiology ; Dose-Response Relationship, Drug ; Ischemic Preconditioning - methods ; Male ; Medical sciences ; Methyl Ethers - administration & dosage ; Neuroprotective Agents - administration & dosage ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species - metabolism ; Up-Regulation - drug effects ; Up-Regulation - physiology</subject><ispartof>Anesthesia and analgesia, 2011-04, Vol.112 (4), p.931-937</ispartof><rights>International Anesthesia Research Society</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4937-e45fc713f76454034664074dde66db59dcfb08f9dbac2c6bf2e068a94860c16f3</citedby><cites>FETCH-LOGICAL-c4937-e45fc713f76454034664074dde66db59dcfb08f9dbac2c6bf2e068a94860c16f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&NEWS=n&CSC=Y&PAGE=fulltext&D=ovft&AN=00000539-201104000-00027$$EHTML$$P50$$Gwolterskluwer$$H</linktohtml><link.rule.ids>314,776,780,4595,27903,27904,65209</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24029773$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21385986$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Qianzi</creatorcontrib><creatorcontrib>Dong, Hui</creatorcontrib><creatorcontrib>Deng, Jiao</creatorcontrib><creatorcontrib>Wang, Qiang</creatorcontrib><creatorcontrib>Ye, Ruidong</creatorcontrib><creatorcontrib>Li, Xuying</creatorcontrib><creatorcontrib>Hu, Sheng</creatorcontrib><creatorcontrib>Dong, Hailong</creatorcontrib><creatorcontrib>Xiong, Lize</creatorcontrib><title>Sevoflurane Preconditioning Induces Neuroprotection Through Reactive Oxygen Species-Mediated Up-Regulation of Antioxidant Enzymes in Rats</title><title>Anesthesia and analgesia</title><addtitle>Anesth Analg</addtitle><description>It has been reported that sevoflurane preconditioning can induce neuroprotection, the mechanisms of which, however, are poorly elucidated. We designed the present study to examine the hypothesis that sevoflurane preconditioning could reduce cerebral ischemia- reperfusion injury through up-regulating antioxidant enzyme activities before ischemic injury by generating reactive oxygen species (ROS).
In preconditioning groups, adult male Sprague-Dawley rats were pretreated with 1 hour sevoflurane exposure at a dose of 1%, 2%, or 4% for 5 consecutive days. At 24 hours after the last exposure, all rats were subjected to focal brain ischemia induced by middle cerebral artery occlusion for 120 minutes followed by 72-hour reperfusion. The role of ROS in ischemic tolerance was assessed by administration of the free radical scavenger dimethylthiourea and antioxidant N-acetylcysteine before each preconditioning. Brain ischemic injury was evaluated by neurologic behavior scores and brain infarct volume calculation. Antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase [GSH-px]) of brain tissue and blood serum were tested at 24 hours after the last sevoflurane preconditioning.
Sevoflurane preconditioning reduced infarct size and improved neurobehavioral outcome in a dose-dependent manner. The neuroprotective effects of sevoflurane preconditioning were abolished by dimethylthiourea and N-acetylcysteine. The activities of catalase and glutathione peroxidase (GSH-px) in the brain tissue were elevated by sevoflurane preconditioning before ischemic injury. The up-regulated activity of GSH-px in serum negatively correlated with brain infarct volume percentage.
Sevoflurane preconditioning induces cerebral ischemic tolerance in a dose- response manner through ROS release and consequent up-regulation of antioxidant enzyme activity before ischemic injury in rats. Serum GSH-px activity could be developed as a marker to assess the effectiveness of sevoflurane preconditioning before ischemia.</description><subject>Anesthesia</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Antioxidants - metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain Ischemia - enzymology</subject><subject>Brain Ischemia - prevention & control</subject><subject>Cerebrovascular Circulation - drug effects</subject><subject>Cerebrovascular Circulation - physiology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Ischemic Preconditioning - methods</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Methyl Ethers - administration & dosage</subject><subject>Neuroprotective Agents - administration & dosage</subject><subject>Random Allocation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Up-Regulation - drug effects</subject><subject>Up-Regulation - physiology</subject><issn>0003-2999</issn><issn>1526-7598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkdFuFCEUhonR2LX6BsZwY7yaCgMDw-Wm2WqT2pptez1h4LCLzsIKM23XN_CtZe1qE0kI58D3nxP-g9BbSk5oTdnH-eXihPSEMmC0rUlvnObP0Iw2tahko9rnaEYIYVWtlDpCr3L-VlJKWvESHRV9WxAxQ7-u4S66YUo6AP6awMRg_ehj8GGFz4OdDGR8CVOK2xRHMPsnfLNOcVqt8RJ0ubgDfPWwW0HA11swHnL1BazXI1h8u62WsJoG_UcWHZ6HEj14q8OIF-HnblOq-4CXesyv0QunhwxvDucxuj1b3Jx-ri6uPp2fzi8qwxWTFfDGGUmZk4I3nDAuBCeSWwtC2L5R1rietE7ZXpvaiN7VQESrFW8FMVQ4dow-PNYtH_oxQR67jc8GhqE4EKfctU0rZdNyWkj-SJoUc07gum3yG512HSXdfgZdmUH3_wyK7N2hwdRvwP4T_TW9AO8PgM5GD654b3x-4jiplZTsqf99HEZI-fsw3UPq1qCHcd2R_WqYqmpCKeElqcquJfsNvpyjgw</recordid><startdate>20110401</startdate><enddate>20110401</enddate><creator>Yang, Qianzi</creator><creator>Dong, Hui</creator><creator>Deng, Jiao</creator><creator>Wang, Qiang</creator><creator>Ye, Ruidong</creator><creator>Li, Xuying</creator><creator>Hu, Sheng</creator><creator>Dong, Hailong</creator><creator>Xiong, Lize</creator><general>International Anesthesia Research Society</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>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20110401</creationdate><title>Sevoflurane Preconditioning Induces Neuroprotection Through Reactive Oxygen Species-Mediated Up-Regulation of Antioxidant Enzymes in Rats</title><author>Yang, Qianzi ; Dong, Hui ; Deng, Jiao ; Wang, Qiang ; Ye, Ruidong ; Li, Xuying ; Hu, Sheng ; Dong, Hailong ; Xiong, Lize</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4937-e45fc713f76454034664074dde66db59dcfb08f9dbac2c6bf2e068a94860c16f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Anesthesia</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Antioxidants - metabolism</topic><topic>Biological and medical sciences</topic><topic>Brain Ischemia - enzymology</topic><topic>Brain Ischemia - prevention & control</topic><topic>Cerebrovascular Circulation - drug effects</topic><topic>Cerebrovascular Circulation - physiology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Ischemic Preconditioning - methods</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Methyl Ethers - administration & dosage</topic><topic>Neuroprotective Agents - administration & dosage</topic><topic>Random Allocation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Up-Regulation - drug effects</topic><topic>Up-Regulation - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Qianzi</creatorcontrib><creatorcontrib>Dong, Hui</creatorcontrib><creatorcontrib>Deng, Jiao</creatorcontrib><creatorcontrib>Wang, Qiang</creatorcontrib><creatorcontrib>Ye, Ruidong</creatorcontrib><creatorcontrib>Li, Xuying</creatorcontrib><creatorcontrib>Hu, Sheng</creatorcontrib><creatorcontrib>Dong, Hailong</creatorcontrib><creatorcontrib>Xiong, Lize</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>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Anesthesia and analgesia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Qianzi</au><au>Dong, Hui</au><au>Deng, Jiao</au><au>Wang, Qiang</au><au>Ye, Ruidong</au><au>Li, Xuying</au><au>Hu, Sheng</au><au>Dong, Hailong</au><au>Xiong, Lize</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sevoflurane Preconditioning Induces Neuroprotection Through Reactive Oxygen Species-Mediated Up-Regulation of Antioxidant Enzymes in Rats</atitle><jtitle>Anesthesia and analgesia</jtitle><addtitle>Anesth Analg</addtitle><date>2011-04-01</date><risdate>2011</risdate><volume>112</volume><issue>4</issue><spage>931</spage><epage>937</epage><pages>931-937</pages><issn>0003-2999</issn><eissn>1526-7598</eissn><coden>AACRAT</coden><abstract>It has been reported that sevoflurane preconditioning can induce neuroprotection, the mechanisms of which, however, are poorly elucidated. We designed the present study to examine the hypothesis that sevoflurane preconditioning could reduce cerebral ischemia- reperfusion injury through up-regulating antioxidant enzyme activities before ischemic injury by generating reactive oxygen species (ROS).
In preconditioning groups, adult male Sprague-Dawley rats were pretreated with 1 hour sevoflurane exposure at a dose of 1%, 2%, or 4% for 5 consecutive days. At 24 hours after the last exposure, all rats were subjected to focal brain ischemia induced by middle cerebral artery occlusion for 120 minutes followed by 72-hour reperfusion. The role of ROS in ischemic tolerance was assessed by administration of the free radical scavenger dimethylthiourea and antioxidant N-acetylcysteine before each preconditioning. Brain ischemic injury was evaluated by neurologic behavior scores and brain infarct volume calculation. Antioxidant enzyme activities (superoxide dismutase, catalase, and glutathione peroxidase [GSH-px]) of brain tissue and blood serum were tested at 24 hours after the last sevoflurane preconditioning.
Sevoflurane preconditioning reduced infarct size and improved neurobehavioral outcome in a dose-dependent manner. The neuroprotective effects of sevoflurane preconditioning were abolished by dimethylthiourea and N-acetylcysteine. The activities of catalase and glutathione peroxidase (GSH-px) in the brain tissue were elevated by sevoflurane preconditioning before ischemic injury. The up-regulated activity of GSH-px in serum negatively correlated with brain infarct volume percentage.
Sevoflurane preconditioning induces cerebral ischemic tolerance in a dose- response manner through ROS release and consequent up-regulation of antioxidant enzyme activity before ischemic injury in rats. Serum GSH-px activity could be developed as a marker to assess the effectiveness of sevoflurane preconditioning before ischemia.</abstract><cop>Hagerstown, MD</cop><pub>International Anesthesia Research Society</pub><pmid>21385986</pmid><doi>10.1213/ANE.0b013e31820bcfa4</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anesthesia Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Antioxidants - metabolism Biological and medical sciences Brain Ischemia - enzymology Brain Ischemia - prevention & control Cerebrovascular Circulation - drug effects Cerebrovascular Circulation - physiology Dose-Response Relationship, Drug Ischemic Preconditioning - methods Male Medical sciences Methyl Ethers - administration & dosage Neuroprotective Agents - administration & dosage Random Allocation Rats Rats, Sprague-Dawley Reactive Oxygen Species - metabolism Up-Regulation - drug effects Up-Regulation - physiology |
| title | Sevoflurane Preconditioning Induces Neuroprotection Through Reactive Oxygen Species-Mediated Up-Regulation of Antioxidant Enzymes in Rats |
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