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Article: Curcumin prevents alcohol-induced liver disease in rats by inhibiting the expression of NF-κB-dependent genes

TitleCurcumin prevents alcohol-induced liver disease in rats by inhibiting the expression of NF-κB-dependent genes
Authors
Issue Date2003
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpgi.physiology.org/
Citation
American Journal Of Physiology - Gastrointestinal And Liver Physiology, 2003, v. 284 n. 2 47-2, p. G321-G327 How to Cite?
AbstractInduction of NF-κB-mediated gene expression has been implicated in the pathogenesis of alcoholic liver disease (ALD). Curcumin, a phenolic antioxidant, inhibits the activation of NF-κB. We determined whether treatment with curcumin would prevent experimental ALD and elucidated the underlying mechanism. Four groups of rats (6 rats/group) were treated by intragastric infusion for 4 wk. One group received fish oil plus ethanol (FE); a second group received fish oil plus dextrose (FD). The third and fourth groups received FE or FD supplemented with 75 mg· kg-1·day-1 of curcumin. Liver samples were analyzed for histopathology, lipid peroxidation, NF-κB binding, TNF-α, IL-12, monocyte chemotactic protein-1, macrophage inflammatory protein-2, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and nitrotyrosine. Rats fed FE developed fatty liver, necrosis, and inflammation, which was accompanied by activation of NF-κB and the induction of cytokines, chemokines, COX-2, iNOS, and nitrotyrosine formation. Treatment with curcumin prevented both the pathological and biochemical changes induced by alcohol. Because endotoxin and the Kupffer cell are implicated in the pathogenesis of ALD, we investigated whether curcumin suppressed the stimulatory effects of endotoxin in isolated Kupffer cells. Curcumin blocked endotoxin-mediated activation of NF-κB and suppressed the expression of cytokines, chemokines, COX-2, and iNOS in Kupffer cells. Thus curcumin prevents experimental ALD, in part by suppressing induction of NF-κB-dependent genes.
Persistent Identifierhttp://hdl.handle.net/10722/149612
ISSN
2015 Impact Factor: 3.297
2015 SCImago Journal Rankings: 1.936
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNanji, AAen_US
dc.contributor.authorJokelainen, Ken_US
dc.contributor.authorTipoe, GLen_US
dc.contributor.authorRahemtulla, Aen_US
dc.contributor.authorThomas, Pen_US
dc.contributor.authorDannenberg, AJen_US
dc.date.accessioned2012-06-26T05:55:58Z-
dc.date.available2012-06-26T05:55:58Z-
dc.date.issued2003en_US
dc.identifier.citationAmerican Journal Of Physiology - Gastrointestinal And Liver Physiology, 2003, v. 284 n. 2 47-2, p. G321-G327en_US
dc.identifier.issn0193-1857en_US
dc.identifier.urihttp://hdl.handle.net/10722/149612-
dc.description.abstractInduction of NF-κB-mediated gene expression has been implicated in the pathogenesis of alcoholic liver disease (ALD). Curcumin, a phenolic antioxidant, inhibits the activation of NF-κB. We determined whether treatment with curcumin would prevent experimental ALD and elucidated the underlying mechanism. Four groups of rats (6 rats/group) were treated by intragastric infusion for 4 wk. One group received fish oil plus ethanol (FE); a second group received fish oil plus dextrose (FD). The third and fourth groups received FE or FD supplemented with 75 mg· kg-1·day-1 of curcumin. Liver samples were analyzed for histopathology, lipid peroxidation, NF-κB binding, TNF-α, IL-12, monocyte chemotactic protein-1, macrophage inflammatory protein-2, cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and nitrotyrosine. Rats fed FE developed fatty liver, necrosis, and inflammation, which was accompanied by activation of NF-κB and the induction of cytokines, chemokines, COX-2, iNOS, and nitrotyrosine formation. Treatment with curcumin prevented both the pathological and biochemical changes induced by alcohol. Because endotoxin and the Kupffer cell are implicated in the pathogenesis of ALD, we investigated whether curcumin suppressed the stimulatory effects of endotoxin in isolated Kupffer cells. Curcumin blocked endotoxin-mediated activation of NF-κB and suppressed the expression of cytokines, chemokines, COX-2, and iNOS in Kupffer cells. Thus curcumin prevents experimental ALD, in part by suppressing induction of NF-κB-dependent genes.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpgi.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Gastrointestinal and Liver Physiologyen_US
dc.subject.meshAlanine Transaminase - Blooden_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - Pharmacologyen_US
dc.subject.meshCentral Nervous System Depressants - Blood - Toxicityen_US
dc.subject.meshCurcumin - Pharmacologyen_US
dc.subject.meshEthanol - Blood - Toxicityen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshInflammation Mediators - Physiologyen_US
dc.subject.meshKupffer Cells - Drug Effects - Physiologyen_US
dc.subject.meshLipid Peroxidation - Drug Effectsen_US
dc.subject.meshLiver - Pathologyen_US
dc.subject.meshLiver Diseases, Alcoholic - Metabolism - Pathology - Prevention & Controlen_US
dc.subject.meshMaleen_US
dc.subject.meshNf-Kappa B - Antagonists & Inhibitors - Biosynthesis - Geneticsen_US
dc.subject.meshRna, Messenger - Biosynthesisen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshThiobarbituric Acid Reactive Substances - Metabolismen_US
dc.titleCurcumin prevents alcohol-induced liver disease in rats by inhibiting the expression of NF-κB-dependent genesen_US
dc.typeArticleen_US
dc.identifier.emailTipoe, GL:tgeorge@hkucc.hku.hken_US
dc.identifier.authorityTipoe, GL=rp00371en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid12388178-
dc.identifier.scopuseid_2-s2.0-0037305472en_US
dc.identifier.hkuros88158-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037305472&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume284en_US
dc.identifier.issue2 47-2en_US
dc.identifier.spageG321en_US
dc.identifier.epageG327en_US
dc.identifier.isiWOS:000180400400018-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridNanji, AA=35885060300en_US
dc.identifier.scopusauthoridJokelainen, K=6603792075en_US
dc.identifier.scopusauthoridTipoe, GL=7003550610en_US
dc.identifier.scopusauthoridRahemtulla, A=7003799325en_US
dc.identifier.scopusauthoridThomas, P=16074032300en_US
dc.identifier.scopusauthoridDannenberg, AJ=7102256248en_US

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