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Article: Effect of mycophenolate mofetil on nitric oxide production and inducible nitric oxide synthase gene expression during renal ischaemia-reperfusion injury

TitleEffect of mycophenolate mofetil on nitric oxide production and inducible nitric oxide synthase gene expression during renal ischaemia-reperfusion injury
Authors
KeywordsIschaemia-reperfusion injury
Mycophenolate mofetil
Nitric oxide
Renal
Issue Date2001
PublisherOxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/
Citation
Nephrology Dialysis Transplantation, 2001, v. 16 n. 8, p. 1577-1582 How to Cite?
AbstractBackground. Recent animal data suggest that inducible nitric oxide synthase (iNOS) derived nitric oxide (NO) plays an important role in the pathogenesis of renal ischaemia-reperfusion injury (IRI) and that inhibition of iNOS ameliorates IRI. Mycophenolate mofetil (MMF), a lymphocyte selective anti-proliferative agent, has been shown to inhibit NO production in vitro. The aim of this study is to evaluate the effect of MMF on NO production and iNOS gene expression in vivo during renal IRI. Methods. Renal IRI was induced by clamping the left renal pedicle of male BALB/c mice for 30 min, followed by 15 min of reperfusion. The mice received placebo or MMF at 40, 80 or 120 mg/kg/day by oral gavage for 5 days before the operation. Sham-operated mice served as the operation control. The amount of NO produced and the level of iNOS gene expression in the kidney tissue during IRI was assessed by spin trapping electron paramagnetic resonance (EPR) spectroscopy and semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) respectively. Results. In the sham-operated kidneys, only low levels of NO and iNOS mRNA were detected. In mice with renal IRI, the amount of NO detected was significantly increased, which was reduced in a dose dependent fashion by pre-treatment with MMF. Pre-treatment with MMF also substantially reduced iNOS gene expression in the kidney tissue. Conclusions. We conclude that pre-treatment with MMF inhibits the production of NO and the induction of iNOS gene expression in the kidney during IRI. These results suggest that MMF might have the potential to ameliorate renal IRI.
Persistent Identifierhttp://hdl.handle.net/10722/78486
ISSN
2015 Impact Factor: 4.085
2015 SCImago Journal Rankings: 1.780
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLui, SLen_HK
dc.contributor.authorChan, LYYen_HK
dc.contributor.authorZhang, XHen_HK
dc.contributor.authorZhu, Wen_HK
dc.contributor.authorChan, TMen_HK
dc.contributor.authorFung, PCWen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2010-09-06T07:43:25Z-
dc.date.available2010-09-06T07:43:25Z-
dc.date.issued2001en_HK
dc.identifier.citationNephrology Dialysis Transplantation, 2001, v. 16 n. 8, p. 1577-1582en_HK
dc.identifier.issn0931-0509en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78486-
dc.description.abstractBackground. Recent animal data suggest that inducible nitric oxide synthase (iNOS) derived nitric oxide (NO) plays an important role in the pathogenesis of renal ischaemia-reperfusion injury (IRI) and that inhibition of iNOS ameliorates IRI. Mycophenolate mofetil (MMF), a lymphocyte selective anti-proliferative agent, has been shown to inhibit NO production in vitro. The aim of this study is to evaluate the effect of MMF on NO production and iNOS gene expression in vivo during renal IRI. Methods. Renal IRI was induced by clamping the left renal pedicle of male BALB/c mice for 30 min, followed by 15 min of reperfusion. The mice received placebo or MMF at 40, 80 or 120 mg/kg/day by oral gavage for 5 days before the operation. Sham-operated mice served as the operation control. The amount of NO produced and the level of iNOS gene expression in the kidney tissue during IRI was assessed by spin trapping electron paramagnetic resonance (EPR) spectroscopy and semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) respectively. Results. In the sham-operated kidneys, only low levels of NO and iNOS mRNA were detected. In mice with renal IRI, the amount of NO detected was significantly increased, which was reduced in a dose dependent fashion by pre-treatment with MMF. Pre-treatment with MMF also substantially reduced iNOS gene expression in the kidney tissue. Conclusions. We conclude that pre-treatment with MMF inhibits the production of NO and the induction of iNOS gene expression in the kidney during IRI. These results suggest that MMF might have the potential to ameliorate renal IRI.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/en_HK
dc.relation.ispartofNephrology Dialysis Transplantationen_HK
dc.rightsNephrology, Dialysis, Transplantation. Copyright © Oxford University Press.en_HK
dc.subjectIschaemia-reperfusion injuryen_HK
dc.subjectMycophenolate mofetilen_HK
dc.subjectNitric oxideen_HK
dc.subjectRenalen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshGene Expression - drug effectsen_HK
dc.subject.meshIschemia - genetics - metabolismen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred BALB Cen_HK
dc.subject.meshMycophenolic Acid - analogs & derivatives - therapeutic useen_HK
dc.subject.meshNitric Oxide - biosynthesisen_HK
dc.subject.meshNitric Oxide Synthase - geneticsen_HK
dc.subject.meshNitric Oxide Synthase Type IIen_HK
dc.subject.meshRenal Circulationen_HK
dc.subject.meshReperfusion Injury - genetics - metabolismen_HK
dc.titleEffect of mycophenolate mofetil on nitric oxide production and inducible nitric oxide synthase gene expression during renal ischaemia-reperfusion injuryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0931-0509&volume=16&issue=8&spage=1577&epage=1582&date=2001&atitle=Effect+of+mycophenolate+mofetil+on+nitric+oxide+production+and+inducible+nitric+oxide+synthase+gene+expression+during+renal+ischaemia-reperfusion+injuryen_HK
dc.identifier.emailChan, TM: dtmchan@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityChan, TM=rp00394en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid11477158en_HK
dc.identifier.scopuseid_2-s2.0-0034877056en_HK
dc.identifier.hkuros61607en_HK
dc.identifier.hkuros74509-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034877056&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume16en_HK
dc.identifier.issue8en_HK
dc.identifier.spage1577en_HK
dc.identifier.epage1582en_HK
dc.identifier.isiWOS:000170410000013-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLui, SL=7102379130en_HK
dc.identifier.scopusauthoridChan, LYY=55182644100en_HK
dc.identifier.scopusauthoridZhang, XH=22837405600en_HK
dc.identifier.scopusauthoridZhu, W=55483193500en_HK
dc.identifier.scopusauthoridChan, TM=7402687700en_HK
dc.identifier.scopusauthoridFung, PCW=7101613315en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK

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