Systemic complement depletion diminishes perihematomal brain edema in rats
The complement cascade is activated after experimental intracerebral hemorrhage (ICH). It remains unclear, however, whether depleting the complement system will improve injury resulting from ICH. This study investigated the effects of systemic complement depletion on brain edema formation after ICH....
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| Veröffentlicht in: | Stroke (1970) 2001, Vol.32 (1), p.162-167 |
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| creator | GUOHUA XI YA HUA KEEP, Richard F YOUNGER, John G HOFF, Julian T |
| description | The complement cascade is activated after experimental intracerebral hemorrhage (ICH). It remains unclear, however, whether depleting the complement system will improve injury resulting from ICH. This study investigated the effects of systemic complement depletion on brain edema formation after ICH.
Fifty-six pentobarbital-anesthetized Sprague-Dawley rats were used. Treatment animals were complement-depleted with cobra venom factor (CVF) (intraperitoneally). Control rats received an equal volume of saline injection (intraperitoneally). In both treatment and control rats, autologous blood (100 microL) was infused stereotaxically into the right basal ganglia. Rats were killed 2, 24, or 72 hours later for brain water, ion, and tumor necrosis factor-alpha (TNF-alpha) measurements, for Western blot analysis, and for immunohistochemical studies. Brain edema was quantitated by wet/dry weight. TNF-alpha levels were measured by enzyme-linked immunosorbent assay. Western blot analysis was applied for C9 semiquantification. Immunohistochemistry was used to detect complement C3d, C5a, C9, and myeloperoxidase.
Perihematomal brain edema was reduced by systemic complement depletion at 24 hours (78.8+/-0.6% versus 81.5+/-0.8% in control, P: |
| doi_str_mv | 10.1161/01.str.32.1.162 |
| format | Article |
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Fifty-six pentobarbital-anesthetized Sprague-Dawley rats were used. Treatment animals were complement-depleted with cobra venom factor (CVF) (intraperitoneally). Control rats received an equal volume of saline injection (intraperitoneally). In both treatment and control rats, autologous blood (100 microL) was infused stereotaxically into the right basal ganglia. Rats were killed 2, 24, or 72 hours later for brain water, ion, and tumor necrosis factor-alpha (TNF-alpha) measurements, for Western blot analysis, and for immunohistochemical studies. Brain edema was quantitated by wet/dry weight. TNF-alpha levels were measured by enzyme-linked immunosorbent assay. Western blot analysis was applied for C9 semiquantification. Immunohistochemistry was used to detect complement C3d, C5a, C9, and myeloperoxidase.
Perihematomal brain edema was reduced by systemic complement depletion at 24 hours (78.8+/-0.6% versus 81.5+/-0.8% in control, P:<0.01) and 72 hours (81.5+/-1.5% versus 83.6+/-0.9% in control, P:<0.05), while cerebellar water content was unaffected (78.2+/-0.3% versus 78.0+/-0. 1%). Complement depletion reduced TNF-alpha production 2 hours after ICH. Immunocytochemistry showed that complement depletion significantly reduced perihematomal C9 deposition, C3d production, and the number of C5a- and myeloperoxidase-positive cells.
Complement depletion by CVF attenuates brain edema in ICH, indicating that complement activation plays an important role in ICH-induced brain edema. Preventing complement activation may be effective in the treatment of ICH.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/01.str.32.1.162</identifier><identifier>PMID: 11136932</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Biological and medical sciences ; Blood Gas Analysis ; Blood Glucose ; Blotting, Western ; Brain - metabolism ; Brain - pathology ; Brain Edema - etiology ; Brain Edema - metabolism ; Brain Edema - pathology ; Brain Edema - therapy ; Cerebral Hemorrhage - complications ; Complement C3d - metabolism ; Complement C5a - metabolism ; Complement C9 - metabolism ; Complement System Proteins - deficiency ; Disease Models, Animal ; Elapid Venoms - administration & dosage ; Enzyme-Linked Immunosorbent Assay ; Hemolysis ; Immunohistochemistry ; Injections, Intraperitoneal ; Male ; Medical sciences ; Neurology ; Peroxidase - metabolism ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha - metabolism ; Vascular diseases and vascular malformations of the nervous system ; Water - analysis ; Water - metabolism</subject><ispartof>Stroke (1970), 2001, Vol.32 (1), p.162-167</ispartof><rights>2001 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Jan 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c582t-2825097e18a7e9ce66090ba568eba7211160ec1f7bf1a11b2fe7888a469dae7b3</citedby><cites>FETCH-LOGICAL-c582t-2825097e18a7e9ce66090ba568eba7211160ec1f7bf1a11b2fe7888a469dae7b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,776,780,785,786,3674,4036,4037,23909,23910,25118,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=862136$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11136932$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>GUOHUA XI</creatorcontrib><creatorcontrib>YA HUA</creatorcontrib><creatorcontrib>KEEP, Richard F</creatorcontrib><creatorcontrib>YOUNGER, John G</creatorcontrib><creatorcontrib>HOFF, Julian T</creatorcontrib><title>Systemic complement depletion diminishes perihematomal brain edema in rats</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>The complement cascade is activated after experimental intracerebral hemorrhage (ICH). It remains unclear, however, whether depleting the complement system will improve injury resulting from ICH. This study investigated the effects of systemic complement depletion on brain edema formation after ICH.
Fifty-six pentobarbital-anesthetized Sprague-Dawley rats were used. Treatment animals were complement-depleted with cobra venom factor (CVF) (intraperitoneally). Control rats received an equal volume of saline injection (intraperitoneally). In both treatment and control rats, autologous blood (100 microL) was infused stereotaxically into the right basal ganglia. Rats were killed 2, 24, or 72 hours later for brain water, ion, and tumor necrosis factor-alpha (TNF-alpha) measurements, for Western blot analysis, and for immunohistochemical studies. Brain edema was quantitated by wet/dry weight. TNF-alpha levels were measured by enzyme-linked immunosorbent assay. Western blot analysis was applied for C9 semiquantification. Immunohistochemistry was used to detect complement C3d, C5a, C9, and myeloperoxidase.
Perihematomal brain edema was reduced by systemic complement depletion at 24 hours (78.8+/-0.6% versus 81.5+/-0.8% in control, P:<0.01) and 72 hours (81.5+/-1.5% versus 83.6+/-0.9% in control, P:<0.05), while cerebellar water content was unaffected (78.2+/-0.3% versus 78.0+/-0. 1%). Complement depletion reduced TNF-alpha production 2 hours after ICH. Immunocytochemistry showed that complement depletion significantly reduced perihematomal C9 deposition, C3d production, and the number of C5a- and myeloperoxidase-positive cells.
Complement depletion by CVF attenuates brain edema in ICH, indicating that complement activation plays an important role in ICH-induced brain edema. Preventing complement activation may be effective in the treatment of ICH.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Gas Analysis</subject><subject>Blood Glucose</subject><subject>Blotting, Western</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain Edema - etiology</subject><subject>Brain Edema - metabolism</subject><subject>Brain Edema - pathology</subject><subject>Brain Edema - therapy</subject><subject>Cerebral Hemorrhage - complications</subject><subject>Complement C3d - metabolism</subject><subject>Complement C5a - metabolism</subject><subject>Complement C9 - metabolism</subject><subject>Complement System Proteins - deficiency</subject><subject>Disease Models, Animal</subject><subject>Elapid Venoms - administration & dosage</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Hemolysis</subject><subject>Immunohistochemistry</subject><subject>Injections, Intraperitoneal</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Peroxidase - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><subject>Water - analysis</subject><subject>Water - metabolism</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0EtLxDAQB_Agirs-zt6kKHhrzaRtmhxl8cmC4OMc0nTKZmnaNWkP--2N7KLgaYbhN8PwJ-QCaAbA4ZZCFkaf5SyDDDg7IHMoWZEWnIlDMqc0lykrpJyRkxDWlFKWi_KYzAAg5zJnc_Lyvg0jOmsSM7hNhw77MWkwdqMd-qSxzvY2rDAkG_R2hU6Pg9NdUntt-wSbOEhi4_UYzshRq7uA5_t6Sj4f7j8WT-ny9fF5cbdMTSnYmDLBSiorBKErlAY5p5LWuuQCa12x-BqnaKCt6hY0QM1arIQQuuCy0VjV-Sm52d3d-OFrwjAqZ4PBrtM9DlNQFS05yAIivPoH18Pk-_ibAlkJCrzkEd3ukPFDCB5btfHWab9VQNVPxoqCev94UzlToGLGceNyf3aqHTZ_fh9qBNd7oIPRXet1b2z4dYKzCPNvolGD6g</recordid><startdate>2001</startdate><enddate>2001</enddate><creator>GUOHUA XI</creator><creator>YA HUA</creator><creator>KEEP, Richard F</creator><creator>YOUNGER, John G</creator><creator>HOFF, Julian T</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>2001</creationdate><title>Systemic complement depletion diminishes perihematomal brain edema in rats</title><author>GUOHUA XI ; YA HUA ; KEEP, Richard F ; YOUNGER, John G ; HOFF, Julian T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c582t-2825097e18a7e9ce66090ba568eba7211160ec1f7bf1a11b2fe7888a469dae7b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Gas Analysis</topic><topic>Blood Glucose</topic><topic>Blotting, Western</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Brain Edema - etiology</topic><topic>Brain Edema - metabolism</topic><topic>Brain Edema - pathology</topic><topic>Brain Edema - therapy</topic><topic>Cerebral Hemorrhage - complications</topic><topic>Complement C3d - metabolism</topic><topic>Complement C5a - metabolism</topic><topic>Complement C9 - metabolism</topic><topic>Complement System Proteins - deficiency</topic><topic>Disease Models, Animal</topic><topic>Elapid Venoms - administration & dosage</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Hemolysis</topic><topic>Immunohistochemistry</topic><topic>Injections, Intraperitoneal</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>Peroxidase - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><topic>Water - analysis</topic><topic>Water - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>GUOHUA XI</creatorcontrib><creatorcontrib>YA HUA</creatorcontrib><creatorcontrib>KEEP, Richard F</creatorcontrib><creatorcontrib>YOUNGER, John G</creatorcontrib><creatorcontrib>HOFF, Julian T</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GUOHUA XI</au><au>YA HUA</au><au>KEEP, Richard F</au><au>YOUNGER, John G</au><au>HOFF, Julian T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Systemic complement depletion diminishes perihematomal brain edema in rats</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>2001</date><risdate>2001</risdate><volume>32</volume><issue>1</issue><spage>162</spage><epage>167</epage><pages>162-167</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>The complement cascade is activated after experimental intracerebral hemorrhage (ICH). It remains unclear, however, whether depleting the complement system will improve injury resulting from ICH. This study investigated the effects of systemic complement depletion on brain edema formation after ICH.
Fifty-six pentobarbital-anesthetized Sprague-Dawley rats were used. Treatment animals were complement-depleted with cobra venom factor (CVF) (intraperitoneally). Control rats received an equal volume of saline injection (intraperitoneally). In both treatment and control rats, autologous blood (100 microL) was infused stereotaxically into the right basal ganglia. Rats were killed 2, 24, or 72 hours later for brain water, ion, and tumor necrosis factor-alpha (TNF-alpha) measurements, for Western blot analysis, and for immunohistochemical studies. Brain edema was quantitated by wet/dry weight. TNF-alpha levels were measured by enzyme-linked immunosorbent assay. Western blot analysis was applied for C9 semiquantification. Immunohistochemistry was used to detect complement C3d, C5a, C9, and myeloperoxidase.
Perihematomal brain edema was reduced by systemic complement depletion at 24 hours (78.8+/-0.6% versus 81.5+/-0.8% in control, P:<0.01) and 72 hours (81.5+/-1.5% versus 83.6+/-0.9% in control, P:<0.05), while cerebellar water content was unaffected (78.2+/-0.3% versus 78.0+/-0. 1%). Complement depletion reduced TNF-alpha production 2 hours after ICH. Immunocytochemistry showed that complement depletion significantly reduced perihematomal C9 deposition, C3d production, and the number of C5a- and myeloperoxidase-positive cells.
Complement depletion by CVF attenuates brain edema in ICH, indicating that complement activation plays an important role in ICH-induced brain edema. Preventing complement activation may be effective in the treatment of ICH.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>11136932</pmid><doi>10.1161/01.str.32.1.162</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection; Journals@Ovid Complete |
| subjects | Animals Biological and medical sciences Blood Gas Analysis Blood Glucose Blotting, Western Brain - metabolism Brain - pathology Brain Edema - etiology Brain Edema - metabolism Brain Edema - pathology Brain Edema - therapy Cerebral Hemorrhage - complications Complement C3d - metabolism Complement C5a - metabolism Complement C9 - metabolism Complement System Proteins - deficiency Disease Models, Animal Elapid Venoms - administration & dosage Enzyme-Linked Immunosorbent Assay Hemolysis Immunohistochemistry Injections, Intraperitoneal Male Medical sciences Neurology Peroxidase - metabolism Rats Rats, Sprague-Dawley Tumor Necrosis Factor-alpha - metabolism Vascular diseases and vascular malformations of the nervous system Water - analysis Water - metabolism |
| title | Systemic complement depletion diminishes perihematomal brain edema in rats |
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