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Article: Effect of celecoxib on experimental liver fibrosis in rat

TitleEffect of celecoxib on experimental liver fibrosis in rat
Authors
Issue Date2006
PublisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1478-3223&site=1
Citation
Liver International, 2006, v. 26 n. 1, p. 125-136 How to Cite?
AbstractBackground/Aim: Cyclooxugenase-2 (COX-2), an inducible enzyme that catalyzes prostaglandin synthesis, has been implicated in a number of hepatic stellate cell (HSC) functions. In the current study, we assessed the in vivo effect of celecoxib, a COX-2-selective inhibitor, in experimental liver fibrosis in rats. Methods: Male Sprague-Dawley rats received experimental treatments for 5 weeks. Serum alanine transminase at the time of sacrifice was measured. Quantitative assessment of liver fibrosis was performed by computerized morphometry. Expression of COX-2, α smooth muscle actin and connective tissue growth factor (CTGF) was evaluated by immunohistochemistry. Real-time quantitative PCR was used to determine the expression of genes associated with fibrogenesis and extracellular matrix degradation. Results: Liver fibrosis was significantly worse in rats that received both carbon tetrachloride (CCl4) and celecoxib, compared with rats that received CCI4 and gavage of water (P=0.037). There was also more HSC activation, and upregulation of collagen α1(I), heat-shock protein 47, αB crystallin, matrix metalloproteinase (MMP)-2, MMP-9 and tissue inhibitor of MMP (TIMP)-2. The expression of TIMP-1 and CTGF was not significantly different between the two groups. The pro-fibrogenic effect of celecoxib in toxin-induced liver fibrosis in rats was further confirmed in thioacetamide model of liver injury. Conclusions: Celecoxib potentiates experimental liver fibrosis; further studies are warranted to investigate the potential pro-fibrogenic effect of celecoxib in other animal models of liver fibrosis and in patients with chronic hepatitis. Copyright © Blackwell Munksgaard 2005.
Persistent Identifierhttp://hdl.handle.net/10722/162966
ISSN
2015 Impact Factor: 4.47
2015 SCImago Journal Rankings: 1.677
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHui, AYen_US
dc.contributor.authorLeung, WKen_US
dc.contributor.authorYuen Chan, HLen_US
dc.contributor.authorChan, FKLen_US
dc.contributor.authorYin Go, MYen_US
dc.contributor.authorChan, KKen_US
dc.contributor.authorTang, BDen_US
dc.contributor.authorChu, ESHen_US
dc.contributor.authorSung, JJYen_US
dc.date.accessioned2012-09-05T05:25:57Z-
dc.date.available2012-09-05T05:25:57Z-
dc.date.issued2006en_US
dc.identifier.citationLiver International, 2006, v. 26 n. 1, p. 125-136en_US
dc.identifier.issn1478-3223en_US
dc.identifier.urihttp://hdl.handle.net/10722/162966-
dc.description.abstractBackground/Aim: Cyclooxugenase-2 (COX-2), an inducible enzyme that catalyzes prostaglandin synthesis, has been implicated in a number of hepatic stellate cell (HSC) functions. In the current study, we assessed the in vivo effect of celecoxib, a COX-2-selective inhibitor, in experimental liver fibrosis in rats. Methods: Male Sprague-Dawley rats received experimental treatments for 5 weeks. Serum alanine transminase at the time of sacrifice was measured. Quantitative assessment of liver fibrosis was performed by computerized morphometry. Expression of COX-2, α smooth muscle actin and connective tissue growth factor (CTGF) was evaluated by immunohistochemistry. Real-time quantitative PCR was used to determine the expression of genes associated with fibrogenesis and extracellular matrix degradation. Results: Liver fibrosis was significantly worse in rats that received both carbon tetrachloride (CCl4) and celecoxib, compared with rats that received CCI4 and gavage of water (P=0.037). There was also more HSC activation, and upregulation of collagen α1(I), heat-shock protein 47, αB crystallin, matrix metalloproteinase (MMP)-2, MMP-9 and tissue inhibitor of MMP (TIMP)-2. The expression of TIMP-1 and CTGF was not significantly different between the two groups. The pro-fibrogenic effect of celecoxib in toxin-induced liver fibrosis in rats was further confirmed in thioacetamide model of liver injury. Conclusions: Celecoxib potentiates experimental liver fibrosis; further studies are warranted to investigate the potential pro-fibrogenic effect of celecoxib in other animal models of liver fibrosis and in patients with chronic hepatitis. Copyright © Blackwell Munksgaard 2005.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1478-3223&site=1en_US
dc.relation.ispartofLiver Internationalen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiopsy, Needleen_US
dc.subject.meshConnective Tissue Growth Factoren_US
dc.subject.meshCyclooxygenase 2 - Analysis - Metabolismen_US
dc.subject.meshCyclooxygenase 2 Inhibitors - Pharmacologyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshDrug Administration Scheduleen_US
dc.subject.meshImmediate-Early Proteins - Analysis - Metabolismen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshIntercellular Signaling Peptides And Proteins - Analysis - Metabolismen_US
dc.subject.meshLiver Cirrhosis, Experimental - Drug Therapy - Pathologyen_US
dc.subject.meshLiver Function Testsen_US
dc.subject.meshMaleen_US
dc.subject.meshMatrix Metalloproteinases - Analysis - Metabolismen_US
dc.subject.meshProbabilityen_US
dc.subject.meshPyrazoles - Pharmacologyen_US
dc.subject.meshRandom Allocationen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSensitivity And Specificityen_US
dc.subject.meshSulfonamides - Pharmacologyen_US
dc.titleEffect of celecoxib on experimental liver fibrosis in raten_US
dc.typeArticleen_US
dc.identifier.emailLeung, WK:waikleung@hku.hken_US
dc.identifier.authorityLeung, WK=rp01479en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1478-3231.2005.01202.xen_US
dc.identifier.pmid16420518en_US
dc.identifier.scopuseid_2-s2.0-33645968418en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33645968418&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume26en_US
dc.identifier.issue1en_US
dc.identifier.spage125en_US
dc.identifier.epage136en_US
dc.identifier.isiWOS:000235135700015-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHui, AY=7102453670en_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridYuen Chan, HL=13005421300en_US
dc.identifier.scopusauthoridChan, FKL=7202586434en_US
dc.identifier.scopusauthoridYin Go, MY=13006257200en_US
dc.identifier.scopusauthoridChan, KK=8599737700en_US
dc.identifier.scopusauthoridTang, BD=7402560876en_US
dc.identifier.scopusauthoridChu, ESH=8631130300en_US
dc.identifier.scopusauthoridSung, JJY=35405352400en_US
dc.identifier.citeulike464067-

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