Neuroprotective effects of infliximab in experimental spinal cord ischemic injury
Abstract Reactive oxygen species (ROS) have been implicated in the pathogenesis of spinal cord injury after both ischemia–reperfusion (I/R) and trauma. This experimental study was designed to investigate the potential effects of infliximab, an anti-tumor necrosis factor-α agent, on I/R injury of the...
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| Veröffentlicht in: | Journal of clinical neuroscience 2010-12, Vol.17 (12), p.1563-1567 |
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| container_title | Journal of clinical neuroscience |
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| creator | Guven, Cagatay Borcek, Alp Ozgun Cemil, Berker Kurt, Gokhan Yildirim, Zuhal Ucankus, Nese Lortlar Kilic, Nedret Ceviker, Necdet |
| description | Abstract Reactive oxygen species (ROS) have been implicated in the pathogenesis of spinal cord injury after both ischemia–reperfusion (I/R) and trauma. This experimental study was designed to investigate the potential effects of infliximab, an anti-tumor necrosis factor-α agent, on I/R injury of the rabbit spinal cord. Eighteen New Zealand white rabbits were divided into three groups, each consisting of six rabbits: sham (no I/R), I/R, and infliximab (I/R + infliximab). Spinal cord ischemia was induced by applying an infrarenal aortic cross clamp for 30 minutes. At 48 hours after ischemia, animals were functionally evaluated using the Tarlov score. Changes in the spinal cord were observed by measuring tissue levels of malondialdehyde (MDA), glutathione (GSH), advanced oxidation protein products (AOPP), and superoxide dismutase (SOD) and by evaluating hematoxylin–eosin-stained sections. At 48 hours after ischemia, the Tarlov scores in the infliximab group were higher than those of the I/R group, MDA and AOPP levels in the I/R group were significantly higher than those in the sham and infliximab groups ( p < 0.05), and SOD levels in the infliximab group were significantly higher than those in the I/R and sham groups ( p < 0.05). The sham group had higher GSH levels than the infliximab group; however, the difference was not statistically significant ( p > 0.05). Histological examination revealed that the infliximab group had significantly less vascular proliferation, edema, and neuron loss than the I/R group. These results indicate that infliximab may protect the spinal cord against injury in a rabbit I/R model. |
| doi_str_mv | 10.1016/j.jocn.2010.04.027 |
| format | Article |
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This experimental study was designed to investigate the potential effects of infliximab, an anti-tumor necrosis factor-α agent, on I/R injury of the rabbit spinal cord. Eighteen New Zealand white rabbits were divided into three groups, each consisting of six rabbits: sham (no I/R), I/R, and infliximab (I/R + infliximab). Spinal cord ischemia was induced by applying an infrarenal aortic cross clamp for 30 minutes. At 48 hours after ischemia, animals were functionally evaluated using the Tarlov score. Changes in the spinal cord were observed by measuring tissue levels of malondialdehyde (MDA), glutathione (GSH), advanced oxidation protein products (AOPP), and superoxide dismutase (SOD) and by evaluating hematoxylin–eosin-stained sections. At 48 hours after ischemia, the Tarlov scores in the infliximab group were higher than those of the I/R group, MDA and AOPP levels in the I/R group were significantly higher than those in the sham and infliximab groups ( p < 0.05), and SOD levels in the infliximab group were significantly higher than those in the I/R and sham groups ( p < 0.05). The sham group had higher GSH levels than the infliximab group; however, the difference was not statistically significant ( p > 0.05). Histological examination revealed that the infliximab group had significantly less vascular proliferation, edema, and neuron loss than the I/R group. These results indicate that infliximab may protect the spinal cord against injury in a rabbit I/R model.</description><identifier>ISSN: 0967-5868</identifier><identifier>EISSN: 1532-2653</identifier><identifier>DOI: 10.1016/j.jocn.2010.04.027</identifier><identifier>PMID: 20817464</identifier><language>eng</language><publisher>Scotland: Elsevier Ltd</publisher><subject>Animal models ; Animals ; Antibodies, Monoclonal - therapeutic use ; Antioxidants ; Glutathione - metabolism ; Infliximab ; Ischemia ; Malondialdehyde - metabolism ; Neurology ; Neurons - metabolism ; Neurons - pathology ; Neuroprotective Agents - therapeutic use ; Oxidative stress ; Rabbits ; Reperfusion injury ; Spinal cord ; Spinal Cord Injuries - drug therapy ; Spinal Cord Injuries - metabolism ; Spinal Cord Injuries - pathology ; Spinal Cord Ischemia - drug therapy ; Spinal Cord Ischemia - metabolism ; Spinal Cord Ischemia - pathology ; Superoxide Dismutase - metabolism</subject><ispartof>Journal of clinical neuroscience, 2010-12, Vol.17 (12), p.1563-1567</ispartof><rights>Elsevier Ltd</rights><rights>2010 Elsevier Ltd</rights><rights>Copyright © 2010 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-abe7acc9768f91534324fe0a037eae0ffc241288f724fed492e98f50c6f3f253</citedby><cites>FETCH-LOGICAL-c508t-abe7acc9768f91534324fe0a037eae0ffc241288f724fed492e98f50c6f3f253</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0967586810003826$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20817464$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guven, Cagatay</creatorcontrib><creatorcontrib>Borcek, Alp Ozgun</creatorcontrib><creatorcontrib>Cemil, Berker</creatorcontrib><creatorcontrib>Kurt, Gokhan</creatorcontrib><creatorcontrib>Yildirim, Zuhal</creatorcontrib><creatorcontrib>Ucankus, Nese Lortlar</creatorcontrib><creatorcontrib>Kilic, Nedret</creatorcontrib><creatorcontrib>Ceviker, Necdet</creatorcontrib><title>Neuroprotective effects of infliximab in experimental spinal cord ischemic injury</title><title>Journal of clinical neuroscience</title><addtitle>J Clin Neurosci</addtitle><description>Abstract Reactive oxygen species (ROS) have been implicated in the pathogenesis of spinal cord injury after both ischemia–reperfusion (I/R) and trauma. This experimental study was designed to investigate the potential effects of infliximab, an anti-tumor necrosis factor-α agent, on I/R injury of the rabbit spinal cord. Eighteen New Zealand white rabbits were divided into three groups, each consisting of six rabbits: sham (no I/R), I/R, and infliximab (I/R + infliximab). Spinal cord ischemia was induced by applying an infrarenal aortic cross clamp for 30 minutes. At 48 hours after ischemia, animals were functionally evaluated using the Tarlov score. Changes in the spinal cord were observed by measuring tissue levels of malondialdehyde (MDA), glutathione (GSH), advanced oxidation protein products (AOPP), and superoxide dismutase (SOD) and by evaluating hematoxylin–eosin-stained sections. At 48 hours after ischemia, the Tarlov scores in the infliximab group were higher than those of the I/R group, MDA and AOPP levels in the I/R group were significantly higher than those in the sham and infliximab groups ( p < 0.05), and SOD levels in the infliximab group were significantly higher than those in the I/R and sham groups ( p < 0.05). The sham group had higher GSH levels than the infliximab group; however, the difference was not statistically significant ( p > 0.05). Histological examination revealed that the infliximab group had significantly less vascular proliferation, edema, and neuron loss than the I/R group. These results indicate that infliximab may protect the spinal cord against injury in a rabbit I/R model.</description><subject>Animal models</subject><subject>Animals</subject><subject>Antibodies, Monoclonal - therapeutic use</subject><subject>Antioxidants</subject><subject>Glutathione - metabolism</subject><subject>Infliximab</subject><subject>Ischemia</subject><subject>Malondialdehyde - metabolism</subject><subject>Neurology</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>Oxidative stress</subject><subject>Rabbits</subject><subject>Reperfusion injury</subject><subject>Spinal cord</subject><subject>Spinal Cord Injuries - drug therapy</subject><subject>Spinal Cord Injuries - metabolism</subject><subject>Spinal Cord Injuries - pathology</subject><subject>Spinal Cord Ischemia - drug therapy</subject><subject>Spinal Cord Ischemia - metabolism</subject><subject>Spinal Cord Ischemia - pathology</subject><subject>Superoxide Dismutase - metabolism</subject><issn>0967-5868</issn><issn>1532-2653</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUuLFTEQhYMoznX0D7iQ3rnqa-XReYAIMviCQRFnH3LTFUzb3bkm3cPcf2-aO7pwoasqinOKqu8Q8pzCngKVr4b9kPy8Z1AHIPbA1AOyox1nLZMdf0h2YKRqOy31BXlSygAARnB4TC4YaKqEFDvy9TOuOR1zWtAv8RYbDKF2pUmhiXMY412c3KG2Dd4dMccJ58WNTTnGuRafct_E4r_jFH0VDWs-PSWPghsLPruvl-Tm_bubq4_t9ZcPn67eXre-A7207oDKeW-U1MHUowVnIiA44AodQgieCcq0Dmqb98IwNDp04GXggXX8krw8r623_1yxLHaqh-A4uhnTWqzpRKcNp-q_SiUZcGrAVCU7K31OpWQM9lg_dvlkKdgNuR3shtxuyC0IW5FX04v79ethwv6P5TfjKnh9FmClcRsx2-Ijzh77mCtq26f47_1v_rL7Mc7Ru_EHnrAMac01imKpLcyC_baFvmVOa9xcM8l_AV4iqBU</recordid><startdate>20101201</startdate><enddate>20101201</enddate><creator>Guven, Cagatay</creator><creator>Borcek, Alp Ozgun</creator><creator>Cemil, Berker</creator><creator>Kurt, Gokhan</creator><creator>Yildirim, Zuhal</creator><creator>Ucankus, Nese Lortlar</creator><creator>Kilic, Nedret</creator><creator>Ceviker, Necdet</creator><general>Elsevier 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><scope>7TK</scope></search><sort><creationdate>20101201</creationdate><title>Neuroprotective effects of infliximab in experimental spinal cord ischemic injury</title><author>Guven, Cagatay ; Borcek, Alp Ozgun ; Cemil, Berker ; Kurt, Gokhan ; Yildirim, Zuhal ; Ucankus, Nese Lortlar ; Kilic, Nedret ; Ceviker, Necdet</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-abe7acc9768f91534324fe0a037eae0ffc241288f724fed492e98f50c6f3f253</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Antibodies, Monoclonal - therapeutic use</topic><topic>Antioxidants</topic><topic>Glutathione - metabolism</topic><topic>Infliximab</topic><topic>Ischemia</topic><topic>Malondialdehyde - metabolism</topic><topic>Neurology</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>Oxidative stress</topic><topic>Rabbits</topic><topic>Reperfusion injury</topic><topic>Spinal cord</topic><topic>Spinal Cord Injuries - drug therapy</topic><topic>Spinal Cord Injuries - metabolism</topic><topic>Spinal Cord Injuries - pathology</topic><topic>Spinal Cord Ischemia - drug therapy</topic><topic>Spinal Cord Ischemia - metabolism</topic><topic>Spinal Cord Ischemia - pathology</topic><topic>Superoxide Dismutase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guven, Cagatay</creatorcontrib><creatorcontrib>Borcek, Alp Ozgun</creatorcontrib><creatorcontrib>Cemil, Berker</creatorcontrib><creatorcontrib>Kurt, Gokhan</creatorcontrib><creatorcontrib>Yildirim, Zuhal</creatorcontrib><creatorcontrib>Ucankus, Nese Lortlar</creatorcontrib><creatorcontrib>Kilic, Nedret</creatorcontrib><creatorcontrib>Ceviker, Necdet</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><collection>Neurosciences Abstracts</collection><jtitle>Journal of clinical neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guven, Cagatay</au><au>Borcek, Alp Ozgun</au><au>Cemil, Berker</au><au>Kurt, Gokhan</au><au>Yildirim, Zuhal</au><au>Ucankus, Nese Lortlar</au><au>Kilic, Nedret</au><au>Ceviker, Necdet</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroprotective effects of infliximab in experimental spinal cord ischemic injury</atitle><jtitle>Journal of clinical neuroscience</jtitle><addtitle>J Clin Neurosci</addtitle><date>2010-12-01</date><risdate>2010</risdate><volume>17</volume><issue>12</issue><spage>1563</spage><epage>1567</epage><pages>1563-1567</pages><issn>0967-5868</issn><eissn>1532-2653</eissn><abstract>Abstract Reactive oxygen species (ROS) have been implicated in the pathogenesis of spinal cord injury after both ischemia–reperfusion (I/R) and trauma. This experimental study was designed to investigate the potential effects of infliximab, an anti-tumor necrosis factor-α agent, on I/R injury of the rabbit spinal cord. Eighteen New Zealand white rabbits were divided into three groups, each consisting of six rabbits: sham (no I/R), I/R, and infliximab (I/R + infliximab). Spinal cord ischemia was induced by applying an infrarenal aortic cross clamp for 30 minutes. At 48 hours after ischemia, animals were functionally evaluated using the Tarlov score. Changes in the spinal cord were observed by measuring tissue levels of malondialdehyde (MDA), glutathione (GSH), advanced oxidation protein products (AOPP), and superoxide dismutase (SOD) and by evaluating hematoxylin–eosin-stained sections. At 48 hours after ischemia, the Tarlov scores in the infliximab group were higher than those of the I/R group, MDA and AOPP levels in the I/R group were significantly higher than those in the sham and infliximab groups ( p < 0.05), and SOD levels in the infliximab group were significantly higher than those in the I/R and sham groups ( p < 0.05). The sham group had higher GSH levels than the infliximab group; however, the difference was not statistically significant ( p > 0.05). Histological examination revealed that the infliximab group had significantly less vascular proliferation, edema, and neuron loss than the I/R group. These results indicate that infliximab may protect the spinal cord against injury in a rabbit I/R model.</abstract><cop>Scotland</cop><pub>Elsevier Ltd</pub><pmid>20817464</pmid><doi>10.1016/j.jocn.2010.04.027</doi><tpages>5</tpages></addata></record> |
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| subjects | Animal models Animals Antibodies, Monoclonal - therapeutic use Antioxidants Glutathione - metabolism Infliximab Ischemia Malondialdehyde - metabolism Neurology Neurons - metabolism Neurons - pathology Neuroprotective Agents - therapeutic use Oxidative stress Rabbits Reperfusion injury Spinal cord Spinal Cord Injuries - drug therapy Spinal Cord Injuries - metabolism Spinal Cord Injuries - pathology Spinal Cord Ischemia - drug therapy Spinal Cord Ischemia - metabolism Spinal Cord Ischemia - pathology Superoxide Dismutase - metabolism |
| title | Neuroprotective effects of infliximab in experimental spinal cord ischemic injury |
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