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Propofol attenuates renal ischemia-reperfusion injury aggravated by hyperglycemia

DC FieldValueLanguage
dc.contributor.author곽영란-
dc.contributor.author심재광-
dc.contributor.author유경종-
dc.contributor.author유영철-
dc.contributor.author임범진-
dc.contributor.author전지혜-
dc.date.accessioned2014-12-18T09:01:06Z-
dc.date.available2014-12-18T09:01:06Z-
dc.date.issued2013-
dc.identifier.issn0022-4804-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/87378-
dc.description.abstractBACKGROUND: Hyperglycemia exacerbates renal ischemia-reperfusion (IR) injury via aggravated inflammatory response and excessive production of reactive oxygen species. This study aimed to investigate the ability of propofol, a known antioxidant, to protect kidneys against IR injury in hyperglycemic rats in comparison with normoglycemic rats. METHODS: Sixty rats were randomly assigned to four groups: normoglycemia-etomidate, normoglycemia-propofol, hyperglycemia-etomidate, and hyperglycemia-propofol. Anesthesia was provided with propofol or etomidate depending on the group. Also, the rats received 1.2 g/kg dextrose or the same volume of normal saline depending on the group. Renal ischemia was induced for 25 min. The rats were killed, and samples were collected 65 min after starting intravenous anesthetics (sham) and 15 min and 24 h after reperfusion injury to compare the histologic degree of renal tubular damage and levels of inflammatory markers and enzymes related to reactive oxygen species. RESULTS: Compared with etomidate, propofol significantly attenuated tubular damage after reperfusion in hyperglycemic rats. Also, tubular damage was greater under hyperglycemia compared with normoglycemia in the etomidate group, whereas it was similar in the propofol group. Propofol preserved superoxide dismutase level and attenuated the increase in levels of myeloperoxidase, interlukin-1β, and tumor necrosis factor-α after reperfusion compared with etomidate especially in hyperglycemic rats. Propofol also attenuated the production of inducible nitric oxide synthase and phosphorylation of inhibitor of κB and nuclear factor-κB after reperfusion, which were more prominent under hyperglycemia. CONCLUSIONS: Propofol conveyed renoprotection against IR injury by preserved antioxidation ability and attenuated inflammatory response, which were more prominent under hyperglycemia.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfJOURNAL OF SURGICAL RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnesthetics, Intravenous/pharmacology-
dc.subject.MESHAnesthetics, Intravenous/therapeutic use-
dc.subject.MESHAnimals-
dc.subject.MESHAntioxidants/pharmacology-
dc.subject.MESHAntioxidants/therapeutic use*-
dc.subject.MESHComorbidity-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHEtomidate/pharmacology-
dc.subject.MESHEtomidate/therapeutic use-
dc.subject.MESHHyperglycemia/epidemiology*-
dc.subject.MESHHyperglycemia/metabolism-
dc.subject.MESHInterleukin-1beta/metabolism-
dc.subject.MESHKidney/blood supply*-
dc.subject.MESHKidney/drug effects-
dc.subject.MESHKidney/metabolism*-
dc.subject.MESHKidney Tubules/drug effects-
dc.subject.MESHKidney Tubules/metabolism-
dc.subject.MESHMale-
dc.subject.MESHNF-kappa B/metabolism-
dc.subject.MESHPeroxidase/metabolism-
dc.subject.MESHPropofol/pharmacology-
dc.subject.MESHPropofol/therapeutic use*-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHReactive Oxygen Species/metabolism-
dc.subject.MESHReperfusion Injury/epidemiology*-
dc.subject.MESHReperfusion Injury/metabolism-
dc.subject.MESHReperfusion Injury/prevention & control*-
dc.subject.MESHSuperoxide Dismutase/metabolism-
dc.subject.MESHTumor Necrosis Factor-alpha/metabolism-
dc.titlePropofol attenuates renal ischemia-reperfusion injury aggravated by hyperglycemia-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pathology (병리학)-
dc.contributor.googleauthorYoung-Chul Yoo-
dc.contributor.googleauthorKyung-Jong Yoo-
dc.contributor.googleauthorBeom Jin Lim-
dc.contributor.googleauthorJi-Hae Jun-
dc.contributor.googleauthorJae-Kwang Shim-
dc.contributor.googleauthorYoung-Lan Kwak-
dc.identifier.doi10.1016/j.jss.2013.02.017-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00172-
dc.contributor.localIdA02205-
dc.contributor.localIdA02453-
dc.contributor.localIdA02484-
dc.contributor.localIdA03363-
dc.contributor.localIdA03551-
dc.relation.journalcodeJ01763-
dc.identifier.eissn1095-8673-
dc.identifier.pmid23498343-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0022480413001029-
dc.subject.keywordAntioxidation-
dc.subject.keywordHyperglycemia-
dc.subject.keywordInflammation-
dc.subject.keywordIschemia/reperfusion-
dc.subject.keywordKidney-
dc.subject.keywordPropofol-
dc.contributor.alternativeNameKwak, Young Lan-
dc.contributor.alternativeNameShim, Jae Kwang-
dc.contributor.alternativeNameYoo, Kyung Jong-
dc.contributor.alternativeNameYoo, Young Chul-
dc.contributor.alternativeNameLim, Beom Jin-
dc.contributor.alternativeNameJun, Ji Hae-
dc.contributor.affiliatedAuthorKwak, Young Lan-
dc.contributor.affiliatedAuthorShim, Jae Kwang-
dc.contributor.affiliatedAuthorYoo, Kyung Jong-
dc.contributor.affiliatedAuthorYoo, Young Chul-
dc.contributor.affiliatedAuthorLim, Beom Jin-
dc.contributor.affiliatedAuthorJun, Ji Hae-
dc.rights.accessRightsnot free-
dc.citation.volume183-
dc.citation.number2-
dc.citation.startPage783-
dc.citation.endPage791-
dc.identifier.bibliographicCitationJOURNAL OF SURGICAL RESEARCH, Vol.183(2) : 783-791, 2013-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Thoracic and Cardiovascular Surgery (흉부외과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Anesthesiology and Pain Medicine (마취통증의학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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