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Delayed treatment with nimesulide reduces measures of oxidative stress following global ischemic brain injury in gerbils
Metabolism of arachidonic acid by cyclooxygenase is one of the primary sources of reactive oxygen species in the ischemic brain. Neuronal overexpression of cyclooxygenase-2 has recently been shown to contribute to neurodegeneration following ischemic injury. In the present study, we examined the pos...
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| Published in: | Neuroscience research 2003-10, Vol.47 (2), p.245-253 |
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| creator | Candelario-Jalil, Eduardo Alvarez, Dalia Merino, Nelson León, Olga Sonia |
| description | Metabolism of arachidonic acid by cyclooxygenase is one of the primary sources of reactive oxygen species in the ischemic brain. Neuronal overexpression of cyclooxygenase-2 has recently been shown to contribute to neurodegeneration following ischemic injury. In the present study, we examined the possibility that the neuroprotective effects of the cyclooxygenase-2 inhibitor nimesulide would depend upon reduction of oxidative stress following cerebral ischemia. Gerbils were subjected to 5 min of transient global cerebral ischemia followed by 48 h of reperfusion and markers of oxidative stress were measured in hippocampus of gerbils receiving vehicle or nimesulide treatment at three different clinically relevant doses (3, 6 or 12 mg/kg). Compared with vehicle, nimesulide significantly (
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| doi_str_mv | 10.1016/S0168-0102(03)00184-6 |
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P<0.05) reduced hippocampal glutathione depletion and lipid peroxidation, as assessed by the levels of malondialdehyde (MDA), 4-hydroxy-alkenals (4-HDA) and lipid hydroperoxides levels, even when the treatment was delayed until 6 h after ischemia. Biochemical evidences of nimesulide neuroprotection were supported by histofluorescence findings using the novel marker of neuronal degeneration Fluoro-Jade B. Few Fluoro-Jade B positive cells were seen in CA1 region of hippocampus in ischemic animals treated with nimesulide compared with vehicle. These results suggest that nimesulide may protect neurons by attenuating oxidative stress and reperfusion injury following the ischemic insult with a wide therapeutic window of protection.</description><identifier>ISSN: 0168-0102</identifier><identifier>EISSN: 1872-8111</identifier><identifier>DOI: 10.1016/S0168-0102(03)00184-6</identifier><identifier>PMID: 14512150</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Animals ; Brain Ischemia - drug therapy ; Brain Ischemia - metabolism ; Cerebral ischemia ; Cyclooxygenase 2 ; Dose-Response Relationship, Drug ; Fluoro-Jade B ; Gerbillinae ; Glutathione ; Isoenzymes - metabolism ; Lipid peroxidation ; Lipid Peroxidation - drug effects ; Lipid Peroxidation - physiology ; Male ; Neurodegeneration ; Nimesulide ; Oxidative stress ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Prostaglandin-Endoperoxide Synthases - metabolism ; Sulfonamides - administration & dosage ; Time Factors</subject><ispartof>Neuroscience research, 2003-10, Vol.47 (2), p.245-253</ispartof><rights>2003 Elsevier Ireland Ltd and the Japan Neuroscience Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c461t-4c8ef7b8151b4846406a6aab529f706156f6dad2528a1f5433197da28289c5713</citedby><cites>FETCH-LOGICAL-c461t-4c8ef7b8151b4846406a6aab529f706156f6dad2528a1f5433197da28289c5713</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0168010203001846$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3535,27903,27904,45759</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14512150$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Candelario-Jalil, Eduardo</creatorcontrib><creatorcontrib>Alvarez, Dalia</creatorcontrib><creatorcontrib>Merino, Nelson</creatorcontrib><creatorcontrib>León, Olga Sonia</creatorcontrib><title>Delayed treatment with nimesulide reduces measures of oxidative stress following global ischemic brain injury in gerbils</title><title>Neuroscience research</title><addtitle>Neurosci Res</addtitle><description>Metabolism of arachidonic acid by cyclooxygenase is one of the primary sources of reactive oxygen species in the ischemic brain. Neuronal overexpression of cyclooxygenase-2 has recently been shown to contribute to neurodegeneration following ischemic injury. In the present study, we examined the possibility that the neuroprotective effects of the cyclooxygenase-2 inhibitor nimesulide would depend upon reduction of oxidative stress following cerebral ischemia. Gerbils were subjected to 5 min of transient global cerebral ischemia followed by 48 h of reperfusion and markers of oxidative stress were measured in hippocampus of gerbils receiving vehicle or nimesulide treatment at three different clinically relevant doses (3, 6 or 12 mg/kg). Compared with vehicle, nimesulide significantly (
P<0.05) reduced hippocampal glutathione depletion and lipid peroxidation, as assessed by the levels of malondialdehyde (MDA), 4-hydroxy-alkenals (4-HDA) and lipid hydroperoxides levels, even when the treatment was delayed until 6 h after ischemia. Biochemical evidences of nimesulide neuroprotection were supported by histofluorescence findings using the novel marker of neuronal degeneration Fluoro-Jade B. Few Fluoro-Jade B positive cells were seen in CA1 region of hippocampus in ischemic animals treated with nimesulide compared with vehicle. These results suggest that nimesulide may protect neurons by attenuating oxidative stress and reperfusion injury following the ischemic insult with a wide therapeutic window of protection.</description><subject>Animals</subject><subject>Brain Ischemia - drug therapy</subject><subject>Brain Ischemia - metabolism</subject><subject>Cerebral ischemia</subject><subject>Cyclooxygenase 2</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fluoro-Jade B</subject><subject>Gerbillinae</subject><subject>Glutathione</subject><subject>Isoenzymes - metabolism</subject><subject>Lipid peroxidation</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Lipid Peroxidation - physiology</subject><subject>Male</subject><subject>Neurodegeneration</subject><subject>Nimesulide</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Prostaglandin-Endoperoxide Synthases - metabolism</subject><subject>Sulfonamides - administration & dosage</subject><subject>Time Factors</subject><issn>0168-0102</issn><issn>1872-8111</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNqFkM1O3DAURi1UBMPQRwB5VbWLUN_EdjwrhGhpkZC6KF1bjn0zGDkxtRNg3r6GGZUlG18vznd_DiEnwM6Agfz6uzyqYsDqz6z5whgoXsk9sgDV1pUCgA9k8R85JEc53zPGmhVvDsghcAE1CLYgz98wmA06OiU004DjRJ_8dEdHP2Ceg3dIE7rZYqYDmjyn8ok9jc_emck_Is0lmDPtYwjxyY9rug6xM4H6bO9w8JZ2yfiR-vF-TptS6BpT50M-Jvu9CRk_7uqS_Ln6fnv5s7r59eP68uKmslzCVHGrsG87BQI6rrjkTBppTCfqVd8yCUL20hlXi1oZ6AVvGli1ztSqVisrWmiW5NO270OKf2fMkx7KahiCGTHOWbcF4qIEl0RsQZtizgl7_ZD8YNJGA9MvyvWrcv3iU7NGvyrXsuROdwPmbkD3lto5LsD5FsBy5qPHpLP1OFp0PqGdtIv-nRH_ALFHkiY</recordid><startdate>20031001</startdate><enddate>20031001</enddate><creator>Candelario-Jalil, Eduardo</creator><creator>Alvarez, Dalia</creator><creator>Merino, Nelson</creator><creator>León, Olga Sonia</creator><general>Elsevier Ireland Ltd</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>7X8</scope></search><sort><creationdate>20031001</creationdate><title>Delayed treatment with nimesulide reduces measures of oxidative stress following global ischemic brain injury in gerbils</title><author>Candelario-Jalil, Eduardo ; Alvarez, Dalia ; Merino, Nelson ; León, Olga Sonia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c461t-4c8ef7b8151b4846406a6aab529f706156f6dad2528a1f5433197da28289c5713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Brain Ischemia - drug therapy</topic><topic>Brain Ischemia - metabolism</topic><topic>Cerebral ischemia</topic><topic>Cyclooxygenase 2</topic><topic>Dose-Response Relationship, Drug</topic><topic>Fluoro-Jade B</topic><topic>Gerbillinae</topic><topic>Glutathione</topic><topic>Isoenzymes - metabolism</topic><topic>Lipid peroxidation</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Lipid Peroxidation - physiology</topic><topic>Male</topic><topic>Neurodegeneration</topic><topic>Nimesulide</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Prostaglandin-Endoperoxide Synthases - metabolism</topic><topic>Sulfonamides - administration & dosage</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Candelario-Jalil, Eduardo</creatorcontrib><creatorcontrib>Alvarez, Dalia</creatorcontrib><creatorcontrib>Merino, Nelson</creatorcontrib><creatorcontrib>León, Olga Sonia</creatorcontrib><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>Neuroscience research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Candelario-Jalil, Eduardo</au><au>Alvarez, Dalia</au><au>Merino, Nelson</au><au>León, Olga Sonia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Delayed treatment with nimesulide reduces measures of oxidative stress following global ischemic brain injury in gerbils</atitle><jtitle>Neuroscience research</jtitle><addtitle>Neurosci Res</addtitle><date>2003-10-01</date><risdate>2003</risdate><volume>47</volume><issue>2</issue><spage>245</spage><epage>253</epage><pages>245-253</pages><issn>0168-0102</issn><eissn>1872-8111</eissn><abstract>Metabolism of arachidonic acid by cyclooxygenase is one of the primary sources of reactive oxygen species in the ischemic brain. 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P<0.05) reduced hippocampal glutathione depletion and lipid peroxidation, as assessed by the levels of malondialdehyde (MDA), 4-hydroxy-alkenals (4-HDA) and lipid hydroperoxides levels, even when the treatment was delayed until 6 h after ischemia. Biochemical evidences of nimesulide neuroprotection were supported by histofluorescence findings using the novel marker of neuronal degeneration Fluoro-Jade B. Few Fluoro-Jade B positive cells were seen in CA1 region of hippocampus in ischemic animals treated with nimesulide compared with vehicle. These results suggest that nimesulide may protect neurons by attenuating oxidative stress and reperfusion injury following the ischemic insult with a wide therapeutic window of protection.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>14512150</pmid><doi>10.1016/S0168-0102(03)00184-6</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Brain Ischemia - drug therapy Brain Ischemia - metabolism Cerebral ischemia Cyclooxygenase 2 Dose-Response Relationship, Drug Fluoro-Jade B Gerbillinae Glutathione Isoenzymes - metabolism Lipid peroxidation Lipid Peroxidation - drug effects Lipid Peroxidation - physiology Male Neurodegeneration Nimesulide Oxidative stress Oxidative Stress - drug effects Oxidative Stress - physiology Prostaglandin-Endoperoxide Synthases - metabolism Sulfonamides - administration & dosage Time Factors |
| title | Delayed treatment with nimesulide reduces measures of oxidative stress following global ischemic brain injury in gerbils |
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