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Article: Arginine reverses ethanol-induced inflammatory and fibrotic changes in liver despite continued ethanol administration

TitleArginine reverses ethanol-induced inflammatory and fibrotic changes in liver despite continued ethanol administration
Authors
Issue Date2001
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org
Citation
Journal Of Pharmacology And Experimental Therapeutics, 2001, v. 299 n. 3, p. 832-839 How to Cite?
AbstractWe investigated the potential of arginine to reverse pathological changes in alcohol-induced liver injury. Four groups (six rats/group) of male Wistar rats were fed a fish oil-ethanol diet for 6 (group 2) or 8 (group 1) weeks. Rats in group 3 were fed fish oil-ethanol for 6 weeks, after which they were administered arginine with fish oil-ethanol for an additional 2 weeks. Rats in group 4 were fed fish oil-dextrose for 8 weeks. Liver samples were analyzed for histopathology, lipid peroxidation, cytochrome P4502E1 activity, nuclear factor-κB, and levels of messenger RNA for tumor necrosis factor-α, cyclooxygenase-2, and inducible nitric oxide synthase. Concentrations of endotoxin were measured in plasma. The most severe inflammation and fibrosis was detected in groups 1 and 2, as were the highest levels of endotoxin, lipid peroxidation, cytochrome P450 2E1 activity, activation of nuclear factor-κB, and mRNA levels for tumor necrosis factor-α, cyclooxygenase-2, and inducible nitric oxide synthase. Plasma nitric oxide was also increased as was nitrotyrosine in liver. After arginine was administered, there was marked improvement in the pathological changes accompanied by decreased levels of endotoxin, lipid peroxidation, activation of nuclear factor-κB, tumor necrosis factor-α, cyclooxygenase-2, inducible nitric oxide, and nitrotyrosine staining. The therapeutic effects of arginine are probably secondary to increased levels of nitric oxide but other effects of arginine cannot be excluded.
Persistent Identifierhttp://hdl.handle.net/10722/67643
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNanji, AAen_HK
dc.contributor.authorJokelainen, Ken_HK
dc.contributor.authorLau, GKKen_HK
dc.contributor.authorRahemtulla, Aen_HK
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorPolavarapu, Ren_HK
dc.contributor.authorLalani, ENen_HK
dc.date.accessioned2010-09-06T05:56:58Z-
dc.date.available2010-09-06T05:56:58Z-
dc.date.issued2001en_HK
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 2001, v. 299 n. 3, p. 832-839en_HK
dc.identifier.issn0022-3565en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67643-
dc.description.abstractWe investigated the potential of arginine to reverse pathological changes in alcohol-induced liver injury. Four groups (six rats/group) of male Wistar rats were fed a fish oil-ethanol diet for 6 (group 2) or 8 (group 1) weeks. Rats in group 3 were fed fish oil-ethanol for 6 weeks, after which they were administered arginine with fish oil-ethanol for an additional 2 weeks. Rats in group 4 were fed fish oil-dextrose for 8 weeks. Liver samples were analyzed for histopathology, lipid peroxidation, cytochrome P4502E1 activity, nuclear factor-κB, and levels of messenger RNA for tumor necrosis factor-α, cyclooxygenase-2, and inducible nitric oxide synthase. Concentrations of endotoxin were measured in plasma. The most severe inflammation and fibrosis was detected in groups 1 and 2, as were the highest levels of endotoxin, lipid peroxidation, cytochrome P450 2E1 activity, activation of nuclear factor-κB, and mRNA levels for tumor necrosis factor-α, cyclooxygenase-2, and inducible nitric oxide synthase. Plasma nitric oxide was also increased as was nitrotyrosine in liver. After arginine was administered, there was marked improvement in the pathological changes accompanied by decreased levels of endotoxin, lipid peroxidation, activation of nuclear factor-κB, tumor necrosis factor-α, cyclooxygenase-2, inducible nitric oxide, and nitrotyrosine staining. The therapeutic effects of arginine are probably secondary to increased levels of nitric oxide but other effects of arginine cannot be excluded.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.orgen_HK
dc.relation.ispartofJournal of Pharmacology and Experimental Therapeuticsen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshArginine - therapeutic useen_HK
dc.subject.meshCyclooxygenase 2en_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshDrug Interactionsen_HK
dc.subject.meshEndotoxins - metabolismen_HK
dc.subject.meshEthanol - toxicityen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInflammation - chemically induced - prevention & controlen_HK
dc.subject.meshIsoenzymes - metabolismen_HK
dc.subject.meshLipid Peroxidation - drug effectsen_HK
dc.subject.meshLiver - drug effects - metabolism - pathologyen_HK
dc.subject.meshLiver Cirrhosis - chemically induced - pathology - prevention & controlen_HK
dc.subject.meshLiver Cirrhosis, Alcoholic - prevention & controlen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMembrane Proteinsen_HK
dc.subject.meshNF-kappa B - metabolismen_HK
dc.subject.meshNitric Oxide - blooden_HK
dc.subject.meshNitric Oxide Synthase - metabolismen_HK
dc.subject.meshNitric Oxide Synthase Type IIen_HK
dc.subject.meshProstaglandin-Endoperoxide Synthases - metabolismen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Wistaren_HK
dc.subject.meshTumor Necrosis Factor-alpha - metabolismen_HK
dc.subject.meshTyrosine - analogs & derivatives - metabolismen_HK
dc.titleArginine reverses ethanol-induced inflammatory and fibrotic changes in liver despite continued ethanol administrationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3565&volume=299&issue=3&spage=832&epage=839&date=2001&atitle=Arginine+reverses+ethanol-induced+inflammatory+and+fibrotic+changes+in+liver+despite+continued+ethanol+administrationen_HK
dc.identifier.emailTipoe, GL:tgeorge@hkucc.hku.hken_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.pmid11714866-
dc.identifier.scopuseid_2-s2.0-0035201477en_HK
dc.identifier.hkuros67755en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035201477&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume299en_HK
dc.identifier.issue3en_HK
dc.identifier.spage832en_HK
dc.identifier.epage839en_HK
dc.identifier.isiWOS:000172484100004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridNanji, AA=35885060300en_HK
dc.identifier.scopusauthoridJokelainen, K=6603792075en_HK
dc.identifier.scopusauthoridLau, GKK=7102301257en_HK
dc.identifier.scopusauthoridRahemtulla, A=7003799325en_HK
dc.identifier.scopusauthoridTipoe, GL=7003550610en_HK
dc.identifier.scopusauthoridPolavarapu, R=6602672737en_HK
dc.identifier.scopusauthoridLalani, EN=7006038297en_HK

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