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Article: FTY720 attenuates hepatic ischemia-reperfusion injury in normal and cirrhotic livers

TitleFTY720 attenuates hepatic ischemia-reperfusion injury in normal and cirrhotic livers
Authors
KeywordsAkt
FTY720
Ischemia-reperfusion injury
Liver cirrhosis
MAPK
Issue Date2005
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/AJT
Citation
American Journal Of Transplantation, 2005, v. 5 n. 1, p. 40-49 How to Cite?
AbstractHepatic ischemia-reperfusion injury is an inevitable consequence during liver surgery. The outcome is particularly poor in cirrhotic livers, which are more prone to hepatic ischemia-reperfusion injury. We aim to study whether FTY720 could attenuate hepatic ischemia-reperfusion injury both in normal and in cirrhotic livers. We applied a 70% liver-ischemia (60 min) model in rats with normal or cirrhotic livers. FTY720 was given 20 min before ischemia and 10 min before reperfusion (1 mg/kg, i.v.). Liver tissues and blood were sampled at 20 min, 60 min, 90 min, 6 h and 24 h after reperfusion for detection of MAPK-Egr-1, Akt pathways and caspase cascade. Hepatic ultrastructure and apoptosis were also compared. FTY720 significantly improved liver function in the rats with normal and cirrhotic livers. Akt pathway was activated at 6 and 24 h after reperfusion. FTY720 significantly down-regulated Egr-1, ET-1, iNOS and MIP-2 accompanied with up-regulation of A20, IL-10, HO-1 and Hsp70. MAPK (Raf-MEK-Erk) pathway was down-regulated. Hepatic ultrastructure was well maintained and fewer apoptotic liver cells were found in the FTY720 groups. In conclusion, FTY720 attenuates ischemia-reperfusion injury in both normal and cirrhotic livers by activation of cell survival Akt signaling and down-regulation of Egr-1 via Raf-MEK-Erk pathway.
Persistent Identifierhttp://hdl.handle.net/10722/84557
ISSN
2015 Impact Factor: 5.669
2015 SCImago Journal Rankings: 2.792
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMan, Ken_HK
dc.contributor.authorNg, KTen_HK
dc.contributor.authorLee, TKen_HK
dc.contributor.authorLo, CMen_HK
dc.contributor.authorSun, CKen_HK
dc.contributor.authorLi, XLen_HK
dc.contributor.authorZhao, Yen_HK
dc.contributor.authorHo, JWen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T08:54:21Z-
dc.date.available2010-09-06T08:54:21Z-
dc.date.issued2005en_HK
dc.identifier.citationAmerican Journal Of Transplantation, 2005, v. 5 n. 1, p. 40-49en_HK
dc.identifier.issn1600-6135en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84557-
dc.description.abstractHepatic ischemia-reperfusion injury is an inevitable consequence during liver surgery. The outcome is particularly poor in cirrhotic livers, which are more prone to hepatic ischemia-reperfusion injury. We aim to study whether FTY720 could attenuate hepatic ischemia-reperfusion injury both in normal and in cirrhotic livers. We applied a 70% liver-ischemia (60 min) model in rats with normal or cirrhotic livers. FTY720 was given 20 min before ischemia and 10 min before reperfusion (1 mg/kg, i.v.). Liver tissues and blood were sampled at 20 min, 60 min, 90 min, 6 h and 24 h after reperfusion for detection of MAPK-Egr-1, Akt pathways and caspase cascade. Hepatic ultrastructure and apoptosis were also compared. FTY720 significantly improved liver function in the rats with normal and cirrhotic livers. Akt pathway was activated at 6 and 24 h after reperfusion. FTY720 significantly down-regulated Egr-1, ET-1, iNOS and MIP-2 accompanied with up-regulation of A20, IL-10, HO-1 and Hsp70. MAPK (Raf-MEK-Erk) pathway was down-regulated. Hepatic ultrastructure was well maintained and fewer apoptotic liver cells were found in the FTY720 groups. In conclusion, FTY720 attenuates ischemia-reperfusion injury in both normal and cirrhotic livers by activation of cell survival Akt signaling and down-regulation of Egr-1 via Raf-MEK-Erk pathway.en_HK
dc.languageengen_HK
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/AJTen_HK
dc.relation.ispartofAmerican Journal of Transplantationen_HK
dc.subjectAkten_HK
dc.subjectFTY720en_HK
dc.subjectIschemia-reperfusion injuryen_HK
dc.subjectLiver cirrhosisen_HK
dc.subjectMAPKen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshChemokine CXCL2en_HK
dc.subject.meshChemokines, CXC - metabolismen_HK
dc.subject.meshDNA Primers - chemistryen_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshEndothelin-1 - metabolismen_HK
dc.subject.meshEpidermal Growth Factor - metabolismen_HK
dc.subject.meshExtracellular Signal-Regulated MAP Kinases - metabolismen_HK
dc.subject.meshFibrosis - drug therapy - pathologyen_HK
dc.subject.meshGene Expression Regulationen_HK
dc.subject.meshHSP70 Heat-Shock Proteins - metabolismen_HK
dc.subject.meshHeme Oxygenase (Decyclizing) - biosynthesisen_HK
dc.subject.meshHeme Oxygenase-1en_HK
dc.subject.meshHepatocytes - cytologyen_HK
dc.subject.meshImmunosuppressive Agents - pharmacologyen_HK
dc.subject.meshIn Situ Nick-End Labelingen_HK
dc.subject.meshInflammationen_HK
dc.subject.meshIntercellular Signaling Peptides and Proteins - metabolismen_HK
dc.subject.meshInterleukin-10 - biosynthesisen_HK
dc.subject.meshLiver - drug effects - injuries - metabolismen_HK
dc.subject.meshMAP Kinase Signaling Systemen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMicroscopy, Electronen_HK
dc.subject.meshNitric Oxide Synthase - metabolismen_HK
dc.subject.meshNitric Oxide Synthase Type IIen_HK
dc.subject.meshPropylene Glycols - pharmacologyen_HK
dc.subject.meshProteins - metabolismen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshReperfusion Injury - drug therapyen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshSignal Transductionen_HK
dc.subject.meshSphingosine - analogs & derivativesen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshUp-Regulationen_HK
dc.subject.meshp38 Mitogen-Activated Protein Kinases - metabolismen_HK
dc.subject.meshraf Kinases - metabolismen_HK
dc.titleFTY720 attenuates hepatic ischemia-reperfusion injury in normal and cirrhotic liversen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1600-6135&volume=5&issue=1&spage=40&epage=49&date=2005&atitle=FTY720+attenuates+hepatic+ischemia-reperfusion+injury+in+normal+and+cirrhotic+liversen_HK
dc.identifier.emailMan, K: kwanman@hku.hken_HK
dc.identifier.emailNg, KT: ledodes@hku.hken_HK
dc.identifier.emailLee, TK: tkwlee@hkucc.hku.hken_HK
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityNg, KT=rp01720en_HK
dc.identifier.authorityLee, TK=rp00447en_HK
dc.identifier.authorityLo, CM=rp00412en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1600-6143.2004.00642.xen_HK
dc.identifier.pmid15636610-
dc.identifier.scopuseid_2-s2.0-11844305973en_HK
dc.identifier.hkuros97135en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-11844305973&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume5en_HK
dc.identifier.issue1en_HK
dc.identifier.spage40en_HK
dc.identifier.epage49en_HK
dc.identifier.isiWOS:000225790600006-
dc.publisher.placeDenmarken_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridNg, KT=7403178513en_HK
dc.identifier.scopusauthoridLee, TK=7501439435en_HK
dc.identifier.scopusauthoridLo, CM=7401771672en_HK
dc.identifier.scopusauthoridSun, CK=7404248685en_HK
dc.identifier.scopusauthoridLi, XL=13008588500en_HK
dc.identifier.scopusauthoridZhao, Y=7407402718en_HK
dc.identifier.scopusauthoridHo, JW=7402649982en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.citeulike67853-

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