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Anti-vascular endothelial growth factor antibody attenuates inflammation and decreases mortality in an experimental model of severe sepsis

DC Field Value Language
dc.contributor.author김준명-
dc.contributor.author김창오-
dc.contributor.author정수진-
dc.contributor.author최준용-
dc.contributor.author한상훈-
dc.date.accessioned2014-12-18T09:51:06Z-
dc.date.available2014-12-18T09:51:06Z-
dc.date.issued2013-
dc.identifier.issn1364-8535-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/88949-
dc.description.abstractINTRODUCTION: Severe sepsis is associated with an unacceptably high rate of mortality. Recent studies revealed elevated levels of vascular endothelial growth factor (VEGF), a potent angiogenic and vascular permeability factor, in patients with sepsis. There was also an association between VEGF levels and sepsis severity. Here we investigate the effects of an anti-VEGF antibody (Bevacizumab, Bev) in an experimental model of sepsis. METHODS: Human umbilical vein endothelial cells (HUVECs), murine cecal ligation and puncture (CLP), and endotoxemia models of sepsis were used. HUVECs were treated with lipopolysaccharide (LPS) and/or Bev, harvested and cytokine mRNA levels determined using a semi-quantitative reverse transcription-polymerase chain reaction assay. The levels of inflammatory cytokine were also determined in HUVECs supernatants. In addition, the effects of Bev on mortality in the CLP and endotoxemia models of sepsis were evaluated. RESULTS: Treatment with Bev and LPS significantly decreased the expression and the level of inflammatory cytokines in HUVECs relative to LPS alone. In CLP and endotoxemia models, survival benefits were evident in mice given 0.1 mg/kg of Bev relative to the CLP or LPS alone (P <0.001 and P = 0.028, respectively), and in 6 h post-treated mice relative to the CLP alone for the effect of different time of Bev (P = 0.033). In addition, Bev treatment inhibited LPS-induced vascular leak in the lung, spleen and kidney in the murine endotoxemia model (P <0.05). CONCLUSIONS: Anti-VEGF antibody may be a promising therapeutic agent due to its beneficial effects on the survival of sepsis by decreasing inflammatory responses and endothelial permeability.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfCRITICAL CARE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHAntibodies, Monoclonal, Humanized/pharmacology-
dc.subject.MESHAntibodies, Monoclonal, Humanized/therapeutic use*-
dc.subject.MESHBevacizumab-
dc.subject.MESHDisease Models, Animal*-
dc.subject.MESHHuman Umbilical Vein Endothelial Cells/drug effects-
dc.subject.MESHHuman Umbilical Vein Endothelial Cells/metabolism-
dc.subject.MESHHumans-
dc.subject.MESHInflammation/drug therapy-
dc.subject.MESHInflammation/metabolism-
dc.subject.MESHInflammation/mortality-
dc.subject.MESHLipopolysaccharides/toxicity-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHSepsis/drug therapy*-
dc.subject.MESHSepsis/metabolism-
dc.subject.MESHSepsis/mortality*-
dc.subject.MESHVascular Endothelial Growth Factor A/antagonists & inhibitors*-
dc.subject.MESHVascular Endothelial Growth Factor A/metabolism-
dc.titleAnti-vascular endothelial growth factor antibody attenuates inflammation and decreases mortality in an experimental model of severe sepsis-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorSu Jin Jeong-
dc.contributor.googleauthorSang Hoon Han-
dc.contributor.googleauthorChang Oh Kim-
dc.contributor.googleauthorJun Yong Choi-
dc.contributor.googleauthorJune Myung Kim-
dc.identifier.doi10.1186/cc12742-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00953-
dc.contributor.localIdA01044-
dc.contributor.localIdA03638-
dc.contributor.localIdA04191-
dc.contributor.localIdA04286-
dc.relation.journalcodeJ00652-
dc.identifier.eissn1466-609X-
dc.identifier.pmid23710641-
dc.subject.keywordsepsis-
dc.subject.keywordvascular endothelial growth factor-
dc.subject.keywordbevacizumab-
dc.subject.keywordanti-VEGF antibody-
dc.contributor.alternativeNameKim, June Myung-
dc.contributor.alternativeNameKim, Chang Oh-
dc.contributor.alternativeNameJeong, Su Jin-
dc.contributor.alternativeNameChoi, Jun Yong-
dc.contributor.alternativeNameHan, Sang Hoon-
dc.contributor.affiliatedAuthorKim, June Myung-
dc.contributor.affiliatedAuthorKim, Chang Oh-
dc.contributor.affiliatedAuthorJeong, Su Jin-
dc.contributor.affiliatedAuthorChoi, Jun Yong-
dc.contributor.affiliatedAuthorHan, Sang Hoon-
dc.rights.accessRightsfree-
dc.citation.volume17-
dc.citation.number3-
dc.citation.startPage97-
dc.identifier.bibliographicCitationCRITICAL CARE, Vol.17(3) : 97, 2013-
dc.identifier.rimsid33697-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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