Neutrophil inhibitory factor is neuroprotective after focal Ischemia in rats
We tested the neuroprotective potential of neutrophil inhibitory factor (rNIF), a novel 41‐kd recombinant glycoprotein derived from a hookworm, in a model of focal cerebral ischemia in the rat. Male Wistar rats were assigned to treatment with rNIF and vehicle. Middle cerebral artery occlusion (MCAO)...
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| Veröffentlicht in: | Annals of neurology 1995-12, Vol.38 (6), p.935-942 |
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| container_title | Annals of neurology |
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| creator | Jiang, Ning Moyle, Matthew Soule, Howard R. Rote, William E. Chopp, Michael |
| description | We tested the neuroprotective potential of neutrophil inhibitory factor (rNIF), a novel 41‐kd recombinant glycoprotein derived from a hookworm, in a model of focal cerebral ischemia in the rat. Male Wistar rats were assigned to treatment with rNIF and vehicle. Middle cerebral artery occlusion (MCAO) for 2 hours was induced by insertion of an intraluminal suture. Infusion of the drug was initiated at the onset of reperfusion. Infarct volume was determined 48 hours after reperfusion. Neutrophils were measured within the ischemic tissue by myeloperoxidase (MPO) staining. Treatment with rNIF resulted in a 48% reduction in cerebral infarction compared with control animals (p < 0.01). Neutrophil accumulation in the ischemic brains of rNIF‐treated rats was reduced significantly (p < 0.01) compared with control animals. The number of neutrophils within the infarcted tissue correlated positively with the size of the area of infarction (p < 0.001, r = 0.6) within representative cerebral coronal sections. We demonstrated a significant neuroprotective effect of rNIF with continuous treatment for 48 hours following 2 hours of MCAO. The neuroprotective effect was correlated with a reduced number of neutrophils within the ischemic tissue. These results demonstrate potential therapeutic properties of rNIF in the management of stroke. |
| doi_str_mv | 10.1002/ana.410380615 |
| format | Article |
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Male Wistar rats were assigned to treatment with rNIF and vehicle. Middle cerebral artery occlusion (MCAO) for 2 hours was induced by insertion of an intraluminal suture. Infusion of the drug was initiated at the onset of reperfusion. Infarct volume was determined 48 hours after reperfusion. Neutrophils were measured within the ischemic tissue by myeloperoxidase (MPO) staining. Treatment with rNIF resulted in a 48% reduction in cerebral infarction compared with control animals (p < 0.01). Neutrophil accumulation in the ischemic brains of rNIF‐treated rats was reduced significantly (p < 0.01) compared with control animals. The number of neutrophils within the infarcted tissue correlated positively with the size of the area of infarction (p < 0.001, r = 0.6) within representative cerebral coronal sections. We demonstrated a significant neuroprotective effect of rNIF with continuous treatment for 48 hours following 2 hours of MCAO. The neuroprotective effect was correlated with a reduced number of neutrophils within the ischemic tissue. These results demonstrate potential therapeutic properties of rNIF in the management of stroke.</description><identifier>ISSN: 0364-5134</identifier><identifier>EISSN: 1531-8249</identifier><identifier>DOI: 10.1002/ana.410380615</identifier><identifier>PMID: 8526467</identifier><identifier>CODEN: ANNED3</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Biological and medical sciences ; Blood Gas Analysis ; Body Weight ; Brain Ischemia - drug therapy ; Glycoproteins - blood ; Glycoproteins - pharmacology ; Helminth Proteins - blood ; Helminth Proteins - pharmacology ; Infusions, Intravenous ; Leukocyte Count ; Male ; Medical sciences ; Membrane Proteins ; Neuropharmacology ; Neuroprotective agent ; Neuroprotective Agents - pharmacology ; Neutrophils - cytology ; Pharmacology. Drug treatments ; Rats ; Rats, Wistar ; Recombinant Proteins - pharmacology ; Reperfusion Injury - drug therapy ; Reperfusion Injury - immunology ; Temperature</subject><ispartof>Annals of neurology, 1995-12, Vol.38 (6), p.935-942</ispartof><rights>Copyright © 1995 American Neurological Association</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4695-17326f49fc60c2a5b0401723458ec0593950dda0ba48dbea17a42976d13762193</citedby><cites>FETCH-LOGICAL-c4695-17326f49fc60c2a5b0401723458ec0593950dda0ba48dbea17a42976d13762193</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fana.410380615$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fana.410380615$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2932279$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8526467$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Ning</creatorcontrib><creatorcontrib>Moyle, Matthew</creatorcontrib><creatorcontrib>Soule, Howard R.</creatorcontrib><creatorcontrib>Rote, William E.</creatorcontrib><creatorcontrib>Chopp, Michael</creatorcontrib><title>Neutrophil inhibitory factor is neuroprotective after focal Ischemia in rats</title><title>Annals of neurology</title><addtitle>Ann Neurol</addtitle><description>We tested the neuroprotective potential of neutrophil inhibitory factor (rNIF), a novel 41‐kd recombinant glycoprotein derived from a hookworm, in a model of focal cerebral ischemia in the rat. Male Wistar rats were assigned to treatment with rNIF and vehicle. Middle cerebral artery occlusion (MCAO) for 2 hours was induced by insertion of an intraluminal suture. Infusion of the drug was initiated at the onset of reperfusion. Infarct volume was determined 48 hours after reperfusion. Neutrophils were measured within the ischemic tissue by myeloperoxidase (MPO) staining. Treatment with rNIF resulted in a 48% reduction in cerebral infarction compared with control animals (p < 0.01). Neutrophil accumulation in the ischemic brains of rNIF‐treated rats was reduced significantly (p < 0.01) compared with control animals. The number of neutrophils within the infarcted tissue correlated positively with the size of the area of infarction (p < 0.001, r = 0.6) within representative cerebral coronal sections. We demonstrated a significant neuroprotective effect of rNIF with continuous treatment for 48 hours following 2 hours of MCAO. The neuroprotective effect was correlated with a reduced number of neutrophils within the ischemic tissue. These results demonstrate potential therapeutic properties of rNIF in the management of stroke.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Gas Analysis</subject><subject>Body Weight</subject><subject>Brain Ischemia - drug therapy</subject><subject>Glycoproteins - blood</subject><subject>Glycoproteins - pharmacology</subject><subject>Helminth Proteins - blood</subject><subject>Helminth Proteins - pharmacology</subject><subject>Infusions, Intravenous</subject><subject>Leukocyte Count</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Proteins</subject><subject>Neuropharmacology</subject><subject>Neuroprotective agent</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neutrophils - cytology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Recombinant Proteins - pharmacology</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - immunology</subject><subject>Temperature</subject><issn>0364-5134</issn><issn>1531-8249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kL1v2zAUxImiReokHTMW0FB0U_r4LY6G0XwgrtshRUfiiaJgprKUklJT__dhYMHI1OkN97t7hyPkgsIlBWBfsMdLQYFXoKh8QxZUclpWTJi3ZAFciVJSLt6T05QeAMAoCifkpJJMCaUXZL3x0xiHx23oitBvQx3GIe6LFl2-RUhF76csx2H0bgx_fYHt6GPRDg674ja5rd8FzM4i4pjOybsWu-Q_zPeM_Lz6er-6Kdffr29Xy3XphDKypJoz1QrTOgWOoaxBANWMC1l5B9JwI6FpEGoUVVN7pBoFM1o1lGvFqOFn5PMhN_f6M_k02l1Izncd9n6YktVaixzDM1geQBeHlKJv7WMMO4x7S8G-rGfzeva4XuY_zsFTvfPNkZ7nyvqnWceUB2gj9i6kI8YMZ0y_9NMH7Cl0fv__n3a5Wb4uMBcOafT_jk6Mv21-r6X9tbm2P5i6Wm2-MXvHnwEAJZW_</recordid><startdate>199512</startdate><enddate>199512</enddate><creator>Jiang, Ning</creator><creator>Moyle, Matthew</creator><creator>Soule, Howard R.</creator><creator>Rote, William E.</creator><creator>Chopp, Michael</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Willey-Liss</general><scope>BSCLL</scope><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>199512</creationdate><title>Neutrophil inhibitory factor is neuroprotective after focal Ischemia in rats</title><author>Jiang, Ning ; Moyle, Matthew ; Soule, Howard R. ; Rote, William E. ; Chopp, Michael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4695-17326f49fc60c2a5b0401723458ec0593950dda0ba48dbea17a42976d13762193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Gas Analysis</topic><topic>Body Weight</topic><topic>Brain Ischemia - drug therapy</topic><topic>Glycoproteins - blood</topic><topic>Glycoproteins - pharmacology</topic><topic>Helminth Proteins - blood</topic><topic>Helminth Proteins - pharmacology</topic><topic>Infusions, Intravenous</topic><topic>Leukocyte Count</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Proteins</topic><topic>Neuropharmacology</topic><topic>Neuroprotective agent</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neutrophils - cytology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Recombinant Proteins - pharmacology</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Reperfusion Injury - immunology</topic><topic>Temperature</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Ning</creatorcontrib><creatorcontrib>Moyle, Matthew</creatorcontrib><creatorcontrib>Soule, Howard R.</creatorcontrib><creatorcontrib>Rote, William E.</creatorcontrib><creatorcontrib>Chopp, Michael</creatorcontrib><collection>Istex</collection><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>Annals of neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Ning</au><au>Moyle, Matthew</au><au>Soule, Howard R.</au><au>Rote, William E.</au><au>Chopp, Michael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neutrophil inhibitory factor is neuroprotective after focal Ischemia in rats</atitle><jtitle>Annals of neurology</jtitle><addtitle>Ann Neurol</addtitle><date>1995-12</date><risdate>1995</risdate><volume>38</volume><issue>6</issue><spage>935</spage><epage>942</epage><pages>935-942</pages><issn>0364-5134</issn><eissn>1531-8249</eissn><coden>ANNED3</coden><abstract>We tested the neuroprotective potential of neutrophil inhibitory factor (rNIF), a novel 41‐kd recombinant glycoprotein derived from a hookworm, in a model of focal cerebral ischemia in the rat. Male Wistar rats were assigned to treatment with rNIF and vehicle. Middle cerebral artery occlusion (MCAO) for 2 hours was induced by insertion of an intraluminal suture. Infusion of the drug was initiated at the onset of reperfusion. Infarct volume was determined 48 hours after reperfusion. Neutrophils were measured within the ischemic tissue by myeloperoxidase (MPO) staining. Treatment with rNIF resulted in a 48% reduction in cerebral infarction compared with control animals (p < 0.01). Neutrophil accumulation in the ischemic brains of rNIF‐treated rats was reduced significantly (p < 0.01) compared with control animals. The number of neutrophils within the infarcted tissue correlated positively with the size of the area of infarction (p < 0.001, r = 0.6) within representative cerebral coronal sections. We demonstrated a significant neuroprotective effect of rNIF with continuous treatment for 48 hours following 2 hours of MCAO. The neuroprotective effect was correlated with a reduced number of neutrophils within the ischemic tissue. These results demonstrate potential therapeutic properties of rNIF in the management of stroke.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>8526467</pmid><doi>10.1002/ana.410380615</doi><tpages>8</tpages></addata></record> |
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| ispartof | Annals of neurology, 1995-12, Vol.38 (6), p.935-942 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Animals Biological and medical sciences Blood Gas Analysis Body Weight Brain Ischemia - drug therapy Glycoproteins - blood Glycoproteins - pharmacology Helminth Proteins - blood Helminth Proteins - pharmacology Infusions, Intravenous Leukocyte Count Male Medical sciences Membrane Proteins Neuropharmacology Neuroprotective agent Neuroprotective Agents - pharmacology Neutrophils - cytology Pharmacology. Drug treatments Rats Rats, Wistar Recombinant Proteins - pharmacology Reperfusion Injury - drug therapy Reperfusion Injury - immunology Temperature |
| title | Neutrophil inhibitory factor is neuroprotective after focal Ischemia in rats |
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