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Neuroprotection by aminoguanidine after lateral fluid-percussive brain injury in rats: a combined magnetic resonance imaging, histopathologic and functional study
The present study examined the effects of a selective inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (AG), on neuronal cell survival and post-traumatic recovery in rats following a lateral fluid percussive brain injury. Daily treatment of AG at the dosage of 100 mg/kg or normal sal...
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Published in: | Neuropharmacology 2003-02, Vol.44 (2), p.253-263 |
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description | The present study examined the effects of a selective inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (AG), on neuronal cell survival and post-traumatic recovery in rats following a lateral fluid percussive brain injury. Daily treatment of AG at the dosage of 100 mg/kg or normal saline was given intraperitoneally into rats starting 2 h before or 30 min after brain injury. Treatment with AG significantly reduced lesion volumes in the brains of rats after injury, as evaluated by high-resolution magnetic resonance imaging (MRI). Immunohistochemical analysis showed a marked induction of iNOS expression in brain macrophages ipsilateral to the injury. Apoptotic neurons were observed in the ipsilateral cerebral cortex by in situ terminal transferase d-UTP nick-end labelling (TUNEL) and caspase-3 immunohistochemistry. In rats receiving prophylactic or post-injury treatment of AG, the number of degenerating neurons was markedly reduced in the cerebrum compared to those receiving saline injection. The location and extent of these pathologic changes correlated with MRI findings. Neurobehavioral studies showed that rotametric performance, grip-strength score, total and ambulatory locomotor responses and acoustic startle response were reduced in rats subjected to the injury but were significantly improved in AG-treated rats. It is suggested that inhibition of iNOS by AG may represent a potential therapeutic strategy for the treatment of traumatic brain injury. |
doi_str_mv | 10.1016/S0028-3908(02)00380-5 |
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Daily treatment of AG at the dosage of 100 mg/kg or normal saline was given intraperitoneally into rats starting 2 h before or 30 min after brain injury. Treatment with AG significantly reduced lesion volumes in the brains of rats after injury, as evaluated by high-resolution magnetic resonance imaging (MRI). Immunohistochemical analysis showed a marked induction of iNOS expression in brain macrophages ipsilateral to the injury. Apoptotic neurons were observed in the ipsilateral cerebral cortex by in situ terminal transferase d-UTP nick-end labelling (TUNEL) and caspase-3 immunohistochemistry. In rats receiving prophylactic or post-injury treatment of AG, the number of degenerating neurons was markedly reduced in the cerebrum compared to those receiving saline injection. The location and extent of these pathologic changes correlated with MRI findings. Neurobehavioral studies showed that rotametric performance, grip-strength score, total and ambulatory locomotor responses and acoustic startle response were reduced in rats subjected to the injury but were significantly improved in AG-treated rats. It is suggested that inhibition of iNOS by AG may represent a potential therapeutic strategy for the treatment of traumatic brain injury.</description><identifier>ISSN: 0028-3908</identifier><identifier>EISSN: 1873-7064</identifier><identifier>DOI: 10.1016/S0028-3908(02)00380-5</identifier><identifier>PMID: 12623224</identifier><identifier>CODEN: NEPHBW</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Aminoguanidine ; Animals ; Antigens, CD ; Antigens, Neoplasm ; Antigens, Surface ; Avian Proteins ; Basigin ; Behaviour ; Biological and medical sciences ; Blood Proteins ; Brain Injuries - drug therapy ; Brain Injuries - pathology ; Brain Injuries - physiopathology ; Caspase 3 ; Caspases - metabolism ; Cerebral Cortex - cytology ; Cerebral Cortex - metabolism ; Cerebral Cortex - physiopathology ; Disease Models, Animal ; Enzyme Inhibitors - therapeutic use ; Guanidines - therapeutic use ; Hand Strength - physiology ; Immunohistochemistry - methods ; In Situ Nick-End Labeling - methods ; Lateral fluid-percussive brain injury ; Magnetic resonance imaging ; Magnetic Resonance Imaging - methods ; Male ; Medical sciences ; Membrane Glycoproteins - metabolism ; Motor Activity - drug effects ; Neuronal apoptosis ; Neuropharmacology ; Neuroprotection ; Neuroprotective agent ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase - genetics ; Nitric Oxide Synthase - metabolism ; Pharmacology. Drug treatments ; Psychomotor Performance - drug effects ; Rats ; Rats, Sprague-Dawley ; Reflex, Acoustic - drug effects ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - analysis ; Time Factors</subject><ispartof>Neuropharmacology, 2003-02, Vol.44 (2), p.253-263</ispartof><rights>2003 Elsevier Science Ltd</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-921d3ff0de8ddb296b7a651540480cd029b2fe881d04f955b786bc58004efc843</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14490617$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12623224$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Jia</creatorcontrib><creatorcontrib>Moochhala, Shabbir</creatorcontrib><creatorcontrib>Shirhan, Md</creatorcontrib><creatorcontrib>Ng, Kian Chye</creatorcontrib><creatorcontrib>Teo, Ai Ling</creatorcontrib><creatorcontrib>Tan, Mui Hong</creatorcontrib><creatorcontrib>Moore, Xiao Lei</creatorcontrib><creatorcontrib>Wong, Meng Cheong</creatorcontrib><creatorcontrib>Ling, Eng Ang</creatorcontrib><title>Neuroprotection by aminoguanidine after lateral fluid-percussive brain injury in rats: a combined magnetic resonance imaging, histopathologic and functional study</title><title>Neuropharmacology</title><addtitle>Neuropharmacology</addtitle><description>The present study examined the effects of a selective inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (AG), on neuronal cell survival and post-traumatic recovery in rats following a lateral fluid percussive brain injury. Daily treatment of AG at the dosage of 100 mg/kg or normal saline was given intraperitoneally into rats starting 2 h before or 30 min after brain injury. Treatment with AG significantly reduced lesion volumes in the brains of rats after injury, as evaluated by high-resolution magnetic resonance imaging (MRI). Immunohistochemical analysis showed a marked induction of iNOS expression in brain macrophages ipsilateral to the injury. Apoptotic neurons were observed in the ipsilateral cerebral cortex by in situ terminal transferase d-UTP nick-end labelling (TUNEL) and caspase-3 immunohistochemistry. In rats receiving prophylactic or post-injury treatment of AG, the number of degenerating neurons was markedly reduced in the cerebrum compared to those receiving saline injection. The location and extent of these pathologic changes correlated with MRI findings. Neurobehavioral studies showed that rotametric performance, grip-strength score, total and ambulatory locomotor responses and acoustic startle response were reduced in rats subjected to the injury but were significantly improved in AG-treated rats. It is suggested that inhibition of iNOS by AG may represent a potential therapeutic strategy for the treatment of traumatic brain injury.</description><subject>Aminoguanidine</subject><subject>Animals</subject><subject>Antigens, CD</subject><subject>Antigens, Neoplasm</subject><subject>Antigens, Surface</subject><subject>Avian Proteins</subject><subject>Basigin</subject><subject>Behaviour</subject><subject>Biological and medical sciences</subject><subject>Blood Proteins</subject><subject>Brain Injuries - drug therapy</subject><subject>Brain Injuries - pathology</subject><subject>Brain Injuries - physiopathology</subject><subject>Caspase 3</subject><subject>Caspases - metabolism</subject><subject>Cerebral Cortex - cytology</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Guanidines - therapeutic use</subject><subject>Hand Strength - physiology</subject><subject>Immunohistochemistry - methods</subject><subject>In Situ Nick-End Labeling - methods</subject><subject>Lateral fluid-percussive brain injury</subject><subject>Magnetic resonance imaging</subject><subject>Magnetic Resonance Imaging - methods</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Motor Activity - drug effects</subject><subject>Neuronal apoptosis</subject><subject>Neuropharmacology</subject><subject>Neuroprotection</subject><subject>Neuroprotective agent</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Psychomotor Performance - drug effects</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reflex, Acoustic - drug effects</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - analysis</subject><subject>Time Factors</subject><issn>0028-3908</issn><issn>1873-7064</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNqFkd9uFCEUh4nR2G31ETTcaGri6IFhZhhvjGn8lzR6oV4TBg5bmlnYAtNkX8cnle5u7GVvOAn5Dpzz-wh5weAdA9a__wXAZdOOIM-BvwFoJTTdI7JicmibAXrxmKz-IyfkNOdrABCSyafkhPGet5yLFfn7A5cUtykWNMXHQKcd1Rsf4nrRwVsfkGpXMNFZ11PP1M2Lt80Wk1ly9rdIp6R9oD5cL2lXC0265A9UUxM3U223dKPXAYs3NGGOQQeD1Nc7H9Zv6ZXPJW51uYpzXFdEB0vdEvaj1M9yWezuGXni9Jzx-bGekT9fPv---NZc_vz6_eLTZWPEIEozcmZb58CitHbiYz8Nuu9YJ-rSYCzwceIOpWQWhBu7bhpkP5lO1lDQGSnaM_L68G5N42bBXNTGZ4PzrAPGJauhhaHnvXwQrAqg6ySrYHcATYo5J3Rqm-rqaacYqDuLam9R3SlSwNXeoupq38vjB8u0QXvfddRWgVdHQGejZ5dqqj7fc0KM0LOhch8PHNbcbj0mlY3HasD6VH0rG_0Do_wDgOW9Pw</recordid><startdate>20030201</startdate><enddate>20030201</enddate><creator>Lu, Jia</creator><creator>Moochhala, Shabbir</creator><creator>Shirhan, Md</creator><creator>Ng, Kian Chye</creator><creator>Teo, Ai Ling</creator><creator>Tan, Mui Hong</creator><creator>Moore, Xiao Lei</creator><creator>Wong, Meng Cheong</creator><creator>Ling, Eng Ang</creator><general>Elsevier Ltd</general><general>Elsevier</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20030201</creationdate><title>Neuroprotection by aminoguanidine after lateral fluid-percussive brain injury in rats: a combined magnetic resonance imaging, histopathologic and functional study</title><author>Lu, Jia ; Moochhala, Shabbir ; Shirhan, Md ; Ng, Kian Chye ; Teo, Ai Ling ; Tan, Mui Hong ; Moore, Xiao Lei ; Wong, Meng Cheong ; Ling, Eng Ang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-921d3ff0de8ddb296b7a651540480cd029b2fe881d04f955b786bc58004efc843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Aminoguanidine</topic><topic>Animals</topic><topic>Antigens, CD</topic><topic>Antigens, Neoplasm</topic><topic>Antigens, Surface</topic><topic>Avian Proteins</topic><topic>Basigin</topic><topic>Behaviour</topic><topic>Biological and medical sciences</topic><topic>Blood Proteins</topic><topic>Brain Injuries - drug therapy</topic><topic>Brain Injuries - pathology</topic><topic>Brain Injuries - physiopathology</topic><topic>Caspase 3</topic><topic>Caspases - metabolism</topic><topic>Cerebral Cortex - cytology</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cerebral Cortex - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Enzyme Inhibitors - therapeutic use</topic><topic>Guanidines - therapeutic use</topic><topic>Hand Strength - physiology</topic><topic>Immunohistochemistry - methods</topic><topic>In Situ Nick-End Labeling - methods</topic><topic>Lateral fluid-percussive brain injury</topic><topic>Magnetic resonance imaging</topic><topic>Magnetic Resonance Imaging - methods</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Motor Activity - drug effects</topic><topic>Neuronal apoptosis</topic><topic>Neuropharmacology</topic><topic>Neuroprotection</topic><topic>Neuroprotective agent</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Psychomotor Performance - drug effects</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reflex, Acoustic - drug effects</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - analysis</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Jia</creatorcontrib><creatorcontrib>Moochhala, Shabbir</creatorcontrib><creatorcontrib>Shirhan, Md</creatorcontrib><creatorcontrib>Ng, Kian Chye</creatorcontrib><creatorcontrib>Teo, Ai Ling</creatorcontrib><creatorcontrib>Tan, Mui Hong</creatorcontrib><creatorcontrib>Moore, Xiao Lei</creatorcontrib><creatorcontrib>Wong, Meng Cheong</creatorcontrib><creatorcontrib>Ling, Eng Ang</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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuropharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Jia</au><au>Moochhala, Shabbir</au><au>Shirhan, Md</au><au>Ng, Kian Chye</au><au>Teo, Ai Ling</au><au>Tan, Mui Hong</au><au>Moore, Xiao Lei</au><au>Wong, Meng Cheong</au><au>Ling, Eng Ang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotection by aminoguanidine after lateral fluid-percussive brain injury in rats: a combined magnetic resonance imaging, histopathologic and functional study</atitle><jtitle>Neuropharmacology</jtitle><addtitle>Neuropharmacology</addtitle><date>2003-02-01</date><risdate>2003</risdate><volume>44</volume><issue>2</issue><spage>253</spage><epage>263</epage><pages>253-263</pages><issn>0028-3908</issn><eissn>1873-7064</eissn><coden>NEPHBW</coden><abstract>The present study examined the effects of a selective inducible nitric oxide synthase (iNOS) inhibitor, aminoguanidine (AG), on neuronal cell survival and post-traumatic recovery in rats following a lateral fluid percussive brain injury. Daily treatment of AG at the dosage of 100 mg/kg or normal saline was given intraperitoneally into rats starting 2 h before or 30 min after brain injury. Treatment with AG significantly reduced lesion volumes in the brains of rats after injury, as evaluated by high-resolution magnetic resonance imaging (MRI). Immunohistochemical analysis showed a marked induction of iNOS expression in brain macrophages ipsilateral to the injury. Apoptotic neurons were observed in the ipsilateral cerebral cortex by in situ terminal transferase d-UTP nick-end labelling (TUNEL) and caspase-3 immunohistochemistry. In rats receiving prophylactic or post-injury treatment of AG, the number of degenerating neurons was markedly reduced in the cerebrum compared to those receiving saline injection. The location and extent of these pathologic changes correlated with MRI findings. Neurobehavioral studies showed that rotametric performance, grip-strength score, total and ambulatory locomotor responses and acoustic startle response were reduced in rats subjected to the injury but were significantly improved in AG-treated rats. It is suggested that inhibition of iNOS by AG may represent a potential therapeutic strategy for the treatment of traumatic brain injury.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>12623224</pmid><doi>10.1016/S0028-3908(02)00380-5</doi><tpages>11</tpages></addata></record> |
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subjects | Aminoguanidine Animals Antigens, CD Antigens, Neoplasm Antigens, Surface Avian Proteins Basigin Behaviour Biological and medical sciences Blood Proteins Brain Injuries - drug therapy Brain Injuries - pathology Brain Injuries - physiopathology Caspase 3 Caspases - metabolism Cerebral Cortex - cytology Cerebral Cortex - metabolism Cerebral Cortex - physiopathology Disease Models, Animal Enzyme Inhibitors - therapeutic use Guanidines - therapeutic use Hand Strength - physiology Immunohistochemistry - methods In Situ Nick-End Labeling - methods Lateral fluid-percussive brain injury Magnetic resonance imaging Magnetic Resonance Imaging - methods Male Medical sciences Membrane Glycoproteins - metabolism Motor Activity - drug effects Neuronal apoptosis Neuropharmacology Neuroprotection Neuroprotective agent Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - genetics Nitric Oxide Synthase - metabolism Pharmacology. Drug treatments Psychomotor Performance - drug effects Rats Rats, Sprague-Dawley Reflex, Acoustic - drug effects Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - analysis Time Factors |
title | Neuroprotection by aminoguanidine after lateral fluid-percussive brain injury in rats: a combined magnetic resonance imaging, histopathologic and functional study |
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