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Article: Endothelial nitric oxide synthase is a critical factor in experimental liver fibrosis

TitleEndothelial nitric oxide synthase is a critical factor in experimental liver fibrosis
Authors
KeywordsCarbon tetrachloride
Chronic liver injury
L-arginine
Nitric oxide synthase
Issue Date2008
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/IEP
Citation
International Journal Of Experimental Pathology, 2008, v. 89 n. 4, p. 241-250 How to Cite?
AbstractReduced expression of endothelial nitric oxide synthase (eNOS) in chronic liver disease can reduce hepatic perfusion and accelerate fibrosis. The relationship between eNOS expression and liver fibrogenesis remains unclear. We investigated whether l-arginine attenuated chronic liver fibrosis through eNOS expression. Chronic liver injury was induced by administration of carbon tetrachloride (CCl4) to mice for 8 weeks. 5-Methylisothiourea hemisulphate (SMT), an iNOS inhibitor, or l-arginine, a NOS substrate were injected subcutaneously. CCl4-induced hepatotoxicity, oxidative stress and accumulation of collagen were detected in the liver. The expression levels of inducible NOS (iNOS) and nuclear factor kappa-B (NF-κB) activity in the liver after CCl4 treatment were increased but eNOS expression and activator protein-1 (AP-1) activity were decreased. Both SMT and l-arginine effectively reduced CCl4 induced oxidative stress and collagen formation, but l-arginine showed a significantly greater suppression of collagen formation, iNOS expression and NF-κB activity. l-Arginine also restored the level of eNOS and AP-1 activity. l-Arginine was more effective than SMT in suppressing liver fibrosis. l-Arginine might improve NO production which facilitates hepatic blood flow and thus retards liver fibrogenesis. Our results showed that the reduced eNOS expression in CCl4-treated mice was reversed by l-arginine. Furthermore, l-arginine also reversed the reduced AP-1 activity, an eNOS promoter. © 2008 The Authors.
Persistent Identifierhttp://hdl.handle.net/10722/149699
ISSN
2015 Impact Factor: 2.125
2015 SCImago Journal Rankings: 0.961
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, TMen_HK
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorLiong, ECen_HK
dc.contributor.authorLau, TYHen_HK
dc.contributor.authorFung, MLen_HK
dc.contributor.authorNanji, AAen_HK
dc.date.accessioned2012-06-26T05:57:16Z-
dc.date.available2012-06-26T05:57:16Z-
dc.date.issued2008en_HK
dc.identifier.citationInternational Journal Of Experimental Pathology, 2008, v. 89 n. 4, p. 241-250en_HK
dc.identifier.issn0959-9673en_HK
dc.identifier.urihttp://hdl.handle.net/10722/149699-
dc.description.abstractReduced expression of endothelial nitric oxide synthase (eNOS) in chronic liver disease can reduce hepatic perfusion and accelerate fibrosis. The relationship between eNOS expression and liver fibrogenesis remains unclear. We investigated whether l-arginine attenuated chronic liver fibrosis through eNOS expression. Chronic liver injury was induced by administration of carbon tetrachloride (CCl4) to mice for 8 weeks. 5-Methylisothiourea hemisulphate (SMT), an iNOS inhibitor, or l-arginine, a NOS substrate were injected subcutaneously. CCl4-induced hepatotoxicity, oxidative stress and accumulation of collagen were detected in the liver. The expression levels of inducible NOS (iNOS) and nuclear factor kappa-B (NF-κB) activity in the liver after CCl4 treatment were increased but eNOS expression and activator protein-1 (AP-1) activity were decreased. Both SMT and l-arginine effectively reduced CCl4 induced oxidative stress and collagen formation, but l-arginine showed a significantly greater suppression of collagen formation, iNOS expression and NF-κB activity. l-Arginine also restored the level of eNOS and AP-1 activity. l-Arginine was more effective than SMT in suppressing liver fibrosis. l-Arginine might improve NO production which facilitates hepatic blood flow and thus retards liver fibrogenesis. Our results showed that the reduced eNOS expression in CCl4-treated mice was reversed by l-arginine. Furthermore, l-arginine also reversed the reduced AP-1 activity, an eNOS promoter. © 2008 The Authors.en_HK
dc.languageengen_US
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/IEPen_HK
dc.relation.ispartofInternational Journal of Experimental Pathologyen_HK
dc.rightsInternational Journal of Experimental Pathology. Copyright © Blackwell Publishing Ltd.-
dc.subjectCarbon tetrachlorideen_HK
dc.subjectChronic liver injuryen_HK
dc.subjectL-arginineen_HK
dc.subjectNitric oxide synthaseen_HK
dc.subject.meshAlanine Transaminase - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArginine - Pharmacologyen_US
dc.subject.meshBlotting, Western - Methodsen_US
dc.subject.meshCarbon Tetrachlorideen_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshDisease Progressionen_US
dc.subject.meshElectrophoretic Mobility Shift Assay - Methodsen_US
dc.subject.meshIsothiuronium - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshLiver - Chemistry - Enzymologyen_US
dc.subject.meshLiver Cirrhosis - Enzymologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Icren_US
dc.subject.meshModels, Animalen_US
dc.subject.meshNf-Kappa B - Analysisen_US
dc.subject.meshNitric Oxide Synthase Type Ii - Analysis - Antagonists & Inhibitors - Geneticsen_US
dc.subject.meshNitric Oxide Synthase Type Iii - Analysis - Genetics - Metabolismen_US
dc.subject.meshOxidative Stressen_US
dc.subject.meshProcollagen - Geneticsen_US
dc.subject.meshRna, Messenger - Analysisen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshTranscription Factor Ap-1 - Analysisen_US
dc.subject.meshTransforming Growth Factor Beta1 - Geneticsen_US
dc.titleEndothelial nitric oxide synthase is a critical factor in experimental liver fibrosisen_HK
dc.typeArticleen_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.emailLeung, TM: leungtm@hkucc.hku.hk-
dc.identifier.emailLiong, EC: eclionga@HKUCC.hku.hk-
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1365-2613.2008.00590.xen_HK
dc.identifier.pmid18429990-
dc.identifier.scopuseid_2-s2.0-47649120300en_HK
dc.identifier.hkuros150967-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-47649120300&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume89en_HK
dc.identifier.issue4en_HK
dc.identifier.spage241en_HK
dc.identifier.epage250en_HK
dc.identifier.isiWOS:000257756100003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLeung, TM=7202110149en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.scopusauthoridLiong, EC=6602732210en_HK
dc.identifier.scopusauthoridLau, TYH=26323763000en_HK
dc.identifier.scopusauthoridFung, ML=7101955092en_HK
dc.identifier.scopusauthoridNanji, AA=35885060300en_HK
dc.identifier.citeulike3024849-

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