Attenuation of Brain Nitrostative and Oxidative Damage by Brain Cooling during Experimental Traumatic Brain Injury
The aim of the present study was to ascertain whether brain cooling causes attenuation of traumatic brain injury by reducing brain nitrostative and oxidative damage. Brain cooling was accomplished by infusion of 5 mL of 4°C saline over 5 minutes via the external jugular vein. Immediately after the o...
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| Veröffentlicht in: | BioMed research international 2011, Vol.2011 (2011), p.1-8 |
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| creator | Lin, Mao- Tsun Lo, Chong-Jeh Chang, Ching-Ping Chio, Chung-Ching Kuo, Jinn-Rung |
| description | The aim of the present study was to ascertain whether brain cooling causes attenuation of traumatic brain injury by reducing brain nitrostative and oxidative damage. Brain cooling was accomplished by infusion of 5 mL of 4°C saline over 5 minutes via the external jugular vein. Immediately after the onset of traumatic brain injury, rats were randomized into two groups and given 37°C or 4°C normal saline. Another group of rats were used as sham operated controls. Behavioral and biochemical assessments were conducted on 72 hours after brain injury or sham operation. As compared to those of the sham-operated controls, the 37°C saline-treated brain injured animals displayed motor deficits, higher cerebral contusion volume and incidence, higher oxidative damage (e.g., lower values of cerebral superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, but higher values of cerebral malondialdehyde), and higher nitrostative damage (e.g., higher values of neuronal nitric oxide synthase and 3-nitrotyrosine). All the motor deficits and brain nitrostative and oxidative damage were significantly reduced by retrograde perfusion of 4°C saline via the jugular vein. Our data suggest that brain cooling may improve the outcomes of traumatic brain injury in rats by reducing brain nitrostative and oxidative damage. |
| doi_str_mv | 10.1155/2011/145214 |
| format | Article |
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Brain cooling was accomplished by infusion of 5 mL of 4°C saline over 5 minutes via the external jugular vein. Immediately after the onset of traumatic brain injury, rats were randomized into two groups and given 37°C or 4°C normal saline. Another group of rats were used as sham operated controls. Behavioral and biochemical assessments were conducted on 72 hours after brain injury or sham operation. As compared to those of the sham-operated controls, the 37°C saline-treated brain injured animals displayed motor deficits, higher cerebral contusion volume and incidence, higher oxidative damage (e.g., lower values of cerebral superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, but higher values of cerebral malondialdehyde), and higher nitrostative damage (e.g., higher values of neuronal nitric oxide synthase and 3-nitrotyrosine). All the motor deficits and brain nitrostative and oxidative damage were significantly reduced by retrograde perfusion of 4°C saline via the jugular vein. Our data suggest that brain cooling may improve the outcomes of traumatic brain injury in rats by reducing brain nitrostative and oxidative damage.</description><identifier>ISSN: 1110-7243</identifier><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 1110-7251</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2011/145214</identifier><identifier>PMID: 21318143</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Puplishing Corporation</publisher><subject>Animals ; Apoptosis ; Behavior ; Biomedical research ; Body Temperature ; Brain - enzymology ; Brain - metabolism ; Brain - pathology ; Brain damage ; Brain Infarction - pathology ; Brain Injuries - enzymology ; Brain Injuries - metabolism ; Brain Injuries - pathology ; Brain Injuries - therapy ; Catalase - metabolism ; Cold ; Experiments ; Glutathione Reductase - metabolism ; Hypothermia, Induced ; Ischemia ; Male ; Malondialdehyde - metabolism ; Medical research ; Nitric Oxide Synthase Type II - metabolism ; Nitrosation ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Rodents ; Studies ; Superoxide Dismutase - metabolism ; Tyrosine - analogs & derivatives ; Tyrosine - metabolism ; Veins & arteries</subject><ispartof>BioMed research international, 2011, Vol.2011 (2011), p.1-8</ispartof><rights>Copyright © 2011 Jinn-Rung Kuo et al.</rights><rights>Copyright © 2011 Jinn-Rung Kuo et al. Jinn-Rung Kuo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2011 Jinn-Rung Kuo et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4454-b123d9c76b2dca1a2d7e02e56b7fd1a0c126605b04e4c4eced582ef6e2f5689a3</citedby><cites>FETCH-LOGICAL-c4454-b123d9c76b2dca1a2d7e02e56b7fd1a0c126605b04e4c4eced582ef6e2f5689a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3034961/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3034961/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,27923,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21318143$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Abdel-Rahman, Abdel A.</contributor><creatorcontrib>Lin, Mao- Tsun</creatorcontrib><creatorcontrib>Lo, Chong-Jeh</creatorcontrib><creatorcontrib>Chang, Ching-Ping</creatorcontrib><creatorcontrib>Chio, Chung-Ching</creatorcontrib><creatorcontrib>Kuo, Jinn-Rung</creatorcontrib><title>Attenuation of Brain Nitrostative and Oxidative Damage by Brain Cooling during Experimental Traumatic Brain Injury</title><title>BioMed research international</title><addtitle>J Biomed Biotechnol</addtitle><description>The aim of the present study was to ascertain whether brain cooling causes attenuation of traumatic brain injury by reducing brain nitrostative and oxidative damage. Brain cooling was accomplished by infusion of 5 mL of 4°C saline over 5 minutes via the external jugular vein. Immediately after the onset of traumatic brain injury, rats were randomized into two groups and given 37°C or 4°C normal saline. Another group of rats were used as sham operated controls. Behavioral and biochemical assessments were conducted on 72 hours after brain injury or sham operation. As compared to those of the sham-operated controls, the 37°C saline-treated brain injured animals displayed motor deficits, higher cerebral contusion volume and incidence, higher oxidative damage (e.g., lower values of cerebral superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, but higher values of cerebral malondialdehyde), and higher nitrostative damage (e.g., higher values of neuronal nitric oxide synthase and 3-nitrotyrosine). All the motor deficits and brain nitrostative and oxidative damage were significantly reduced by retrograde perfusion of 4°C saline via the jugular vein. Our data suggest that brain cooling may improve the outcomes of traumatic brain injury in rats by reducing brain nitrostative and oxidative damage.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Behavior</subject><subject>Biomedical research</subject><subject>Body Temperature</subject><subject>Brain - enzymology</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain damage</subject><subject>Brain Infarction - pathology</subject><subject>Brain Injuries - enzymology</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Injuries - pathology</subject><subject>Brain Injuries - therapy</subject><subject>Catalase - metabolism</subject><subject>Cold</subject><subject>Experiments</subject><subject>Glutathione Reductase - metabolism</subject><subject>Hypothermia, Induced</subject><subject>Ischemia</subject><subject>Male</subject><subject>Malondialdehyde - metabolism</subject><subject>Medical research</subject><subject>Nitric Oxide Synthase Type II - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Mao- Tsun</au><au>Lo, Chong-Jeh</au><au>Chang, Ching-Ping</au><au>Chio, Chung-Ching</au><au>Kuo, Jinn-Rung</au><au>Abdel-Rahman, Abdel A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Attenuation of Brain Nitrostative and Oxidative Damage by Brain Cooling during Experimental Traumatic Brain Injury</atitle><jtitle>BioMed research international</jtitle><addtitle>J Biomed Biotechnol</addtitle><date>2011</date><risdate>2011</risdate><volume>2011</volume><issue>2011</issue><spage>1</spage><epage>8</epage><pages>1-8</pages><issn>1110-7243</issn><issn>2314-6133</issn><eissn>1110-7251</eissn><eissn>2314-6141</eissn><abstract>The aim of the present study was to ascertain whether brain cooling causes attenuation of traumatic brain injury by reducing brain nitrostative and oxidative damage. Brain cooling was accomplished by infusion of 5 mL of 4°C saline over 5 minutes via the external jugular vein. Immediately after the onset of traumatic brain injury, rats were randomized into two groups and given 37°C or 4°C normal saline. Another group of rats were used as sham operated controls. Behavioral and biochemical assessments were conducted on 72 hours after brain injury or sham operation. As compared to those of the sham-operated controls, the 37°C saline-treated brain injured animals displayed motor deficits, higher cerebral contusion volume and incidence, higher oxidative damage (e.g., lower values of cerebral superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase, but higher values of cerebral malondialdehyde), and higher nitrostative damage (e.g., higher values of neuronal nitric oxide synthase and 3-nitrotyrosine). All the motor deficits and brain nitrostative and oxidative damage were significantly reduced by retrograde perfusion of 4°C saline via the jugular vein. Our data suggest that brain cooling may improve the outcomes of traumatic brain injury in rats by reducing brain nitrostative and oxidative damage.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Puplishing Corporation</pub><pmid>21318143</pmid><doi>10.1155/2011/145214</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Apoptosis Behavior Biomedical research Body Temperature Brain - enzymology Brain - metabolism Brain - pathology Brain damage Brain Infarction - pathology Brain Injuries - enzymology Brain Injuries - metabolism Brain Injuries - pathology Brain Injuries - therapy Catalase - metabolism Cold Experiments Glutathione Reductase - metabolism Hypothermia, Induced Ischemia Male Malondialdehyde - metabolism Medical research Nitric Oxide Synthase Type II - metabolism Nitrosation Oxidative Stress Rats Rats, Sprague-Dawley Rodents Studies Superoxide Dismutase - metabolism Tyrosine - analogs & derivatives Tyrosine - metabolism Veins & arteries |
| title | Attenuation of Brain Nitrostative and Oxidative Damage by Brain Cooling during Experimental Traumatic Brain Injury |
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