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Article: Effect of rapamycin on renal ischemia-reperfusion injury in mice

TitleEffect of rapamycin on renal ischemia-reperfusion injury in mice
Authors
KeywordsIschemia-reperfusion injury
Rapamycin
Renal
Tubular cells
Issue Date2006
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journal.asp?ref=0934-0874&site=1
Citation
Transplant International, 2006, v. 19 n. 10, p. 834-839 How to Cite?
AbstractThe aim of this study was to determine the effect of rapamycin on renal ischemia-reperfusion injury (IRI) in mice. Renal IRI was induced in male BALB/c mice by clamping both renal pedicles for 45 min. The mice were treated with either vehicle or rapamycin (2 mg/kg/day) by oral gavage, starting 1 day before the IRI and continued daily till killing. The mice were killed on days 1, 3 and 7 after the operation. The severity of the renal IRI was assessed by serum creatinine levels and renal histology. Proliferation of renal tubular cells was quantified by immunohistochemical staining for proliferating cell nuclear antigen (PCNA). One day after the IRI, the serum creatinine levels of rapamycin-treated mice were significantly higher than those of the vehicle-treated mice. Kidney sections from rapamycin-treated mice showed more marked tubular damage and significantly lower number of PCNA-positive cells. The number of PCNA-positive cells in the rapamycin-treated mice remained significantly lower on day 3 after the IRI. By day 7 after the IRI, the serum creatinine levels, renal histology and positive PCNA staining in the kidney sections became similar between the two treatment groups. We conclude that in this murine model of renal IRI, rapamycin treatment aggravates renal IRI during the first 3 days after the insult. This effect might be mediated, at least partly, through inhibition of renal tubular cell proliferation. © 2006 The Authors.
Persistent Identifierhttp://hdl.handle.net/10722/77930
ISSN
2023 Impact Factor: 2.7
2023 SCImago Journal Rankings: 0.899
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLui, SLen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorTsang, Ren_HK
dc.contributor.authorYung, Sen_HK
dc.contributor.authorLai, KNen_HK
dc.contributor.authorChan, TMen_HK
dc.date.accessioned2010-09-06T07:37:19Z-
dc.date.available2010-09-06T07:37:19Z-
dc.date.issued2006en_HK
dc.identifier.citationTransplant International, 2006, v. 19 n. 10, p. 834-839en_HK
dc.identifier.issn0934-0874en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77930-
dc.description.abstractThe aim of this study was to determine the effect of rapamycin on renal ischemia-reperfusion injury (IRI) in mice. Renal IRI was induced in male BALB/c mice by clamping both renal pedicles for 45 min. The mice were treated with either vehicle or rapamycin (2 mg/kg/day) by oral gavage, starting 1 day before the IRI and continued daily till killing. The mice were killed on days 1, 3 and 7 after the operation. The severity of the renal IRI was assessed by serum creatinine levels and renal histology. Proliferation of renal tubular cells was quantified by immunohistochemical staining for proliferating cell nuclear antigen (PCNA). One day after the IRI, the serum creatinine levels of rapamycin-treated mice were significantly higher than those of the vehicle-treated mice. Kidney sections from rapamycin-treated mice showed more marked tubular damage and significantly lower number of PCNA-positive cells. The number of PCNA-positive cells in the rapamycin-treated mice remained significantly lower on day 3 after the IRI. By day 7 after the IRI, the serum creatinine levels, renal histology and positive PCNA staining in the kidney sections became similar between the two treatment groups. We conclude that in this murine model of renal IRI, rapamycin treatment aggravates renal IRI during the first 3 days after the insult. This effect might be mediated, at least partly, through inhibition of renal tubular cell proliferation. © 2006 The Authors.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journal.asp?ref=0934-0874&site=1en_HK
dc.relation.ispartofTransplant Internationalen_HK
dc.rightsTransplant International. Copyright © Blackwell Publishing Ltd.en_HK
dc.subjectIschemia-reperfusion injuryen_HK
dc.subjectRapamycinen_HK
dc.subjectRenalen_HK
dc.subjectTubular cellsen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshCreatinine - blooden_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshImmunosuppressive Agents - pharmacologyen_HK
dc.subject.meshKidney - metabolism - pathologyen_HK
dc.subject.meshKidney Diseases - drug therapy - therapyen_HK
dc.subject.meshKidney Transplantationen_HK
dc.subject.meshKidney Tubules - cytologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred BALB Cen_HK
dc.subject.meshReperfusion Injury - pathologyen_HK
dc.subject.meshSirolimus - pharmacologyen_HK
dc.titleEffect of rapamycin on renal ischemia-reperfusion injury in miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0934-0874&volume=19&spage=834&epage=839&date=2006&atitle=Effect+of+rapamycin+on+renal+ischemia-reperfusion+injury+in+miceen_HK
dc.identifier.emailChan, KW: hrmtckw@hku.hken_HK
dc.identifier.emailYung, S: ssyyung@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.emailChan, TM: dtmchan@hku.hken_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityYung, S=rp00455en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.identifier.authorityChan, TM=rp00394en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1432-2277.2006.00361.xen_HK
dc.identifier.pmid16961776-
dc.identifier.scopuseid_2-s2.0-33748488439en_HK
dc.identifier.hkuros121670en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33748488439&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume19en_HK
dc.identifier.issue10en_HK
dc.identifier.spage834en_HK
dc.identifier.epage839en_HK
dc.identifier.isiWOS:000240350600009-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLui, SL=7102379130en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridTsang, R=36808555100en_HK
dc.identifier.scopusauthoridYung, S=22636568800en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK
dc.identifier.scopusauthoridChan, TM=7402687700en_HK
dc.identifier.citeulike834377-
dc.identifier.issnl0934-0874-

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