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Article: Cyclooxygenase inhibitors protect d-galactosamine/lipopolysaccharide induced acute hepatic injury in experimental mice model

TitleCyclooxygenase inhibitors protect d-galactosamine/lipopolysaccharide induced acute hepatic injury in experimental mice model
Authors
KeywordsAcute Liver Injury
Cyclooxygenase Inhibitor
Lipopolysaccharide
Oxidative Stress
Issue Date2012
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/foodchemtox
Citation
Food And Chemical Toxicology, 2012, v. 50 n. 3-4, p. 861-866 How to Cite?
AbstractWe investigated the protective effects of two non-steroid anti-inflammatory drugs, indomethacin (COX-1 and COX-2 inhibitors) and nimesulide (specific COX-2 inhibitor) on the hepatic injury induced by lipopolysaccharide in d-galactosamine sensitized (Gal/LPS) mice. ICR male mice were injected with a single dose of Gal/LPS with or without pre-treatment of 3. mg/kg indomethacin or 30. mg/kg nimesulide (single i.p. injection). Sixteen hours later, blood and liver tissues of mice were collected for histological, molecular, and biochemical analyses. Our results showed marked reduction of hepatic necrosis, serum ALT, and tissue TBARS levels in both indomethacin- and nimesulide-pre-treated mice when compared with Gal/LPS-treated mice. Western blot and RT-PCR analysis showed decreased levels of iNOS mRNA, iNOS protein, and nitrotyrosine formation in both COX inhibitor pre-treated groups when compared with Gal/LPS-treated group. There was an inverse relationship between COX-1 and COX-2 expressions, as well as between COX-2 and C/EBP-α expressions in COX inhibitors groups, Gal/LPS and control groups. COX inhibitors reduced the expression of TNF-α mRNA and the activity of NF-κB which were elevated by Gal/LPS treatment. We conclude that COX inhibitors protected the liver from Gal/LPS-induced hepatotoxicity. COX inhibitors could be considered as potential agents in the prevention of acute liver failure and sepsis. © 2011 Elsevier Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/149779
ISSN
2015 Impact Factor: 3.584
2015 SCImago Journal Rankings: 1.190
ISI Accession Number ID
Funding AgencyGrant Number
University Research Committee, The University of Hong Kong, Hong Kong
Funding Information:

This study was supported by Small Project Funding, University Research Committee, The University of Hong Kong, Hong Kong.

References

 

DC FieldValueLanguage
dc.contributor.authorLiong, ECen_US
dc.contributor.authorXiao, Jen_US
dc.contributor.authorLau, TYHen_US
dc.contributor.authorNanji, AAen_US
dc.contributor.authorTipoe, GLen_US
dc.date.accessioned2012-06-26T05:58:29Z-
dc.date.available2012-06-26T05:58:29Z-
dc.date.issued2012en_US
dc.identifier.citationFood And Chemical Toxicology, 2012, v. 50 n. 3-4, p. 861-866en_US
dc.identifier.issn0278-6915en_US
dc.identifier.urihttp://hdl.handle.net/10722/149779-
dc.description.abstractWe investigated the protective effects of two non-steroid anti-inflammatory drugs, indomethacin (COX-1 and COX-2 inhibitors) and nimesulide (specific COX-2 inhibitor) on the hepatic injury induced by lipopolysaccharide in d-galactosamine sensitized (Gal/LPS) mice. ICR male mice were injected with a single dose of Gal/LPS with or without pre-treatment of 3. mg/kg indomethacin or 30. mg/kg nimesulide (single i.p. injection). Sixteen hours later, blood and liver tissues of mice were collected for histological, molecular, and biochemical analyses. Our results showed marked reduction of hepatic necrosis, serum ALT, and tissue TBARS levels in both indomethacin- and nimesulide-pre-treated mice when compared with Gal/LPS-treated mice. Western blot and RT-PCR analysis showed decreased levels of iNOS mRNA, iNOS protein, and nitrotyrosine formation in both COX inhibitor pre-treated groups when compared with Gal/LPS-treated group. There was an inverse relationship between COX-1 and COX-2 expressions, as well as between COX-2 and C/EBP-α expressions in COX inhibitors groups, Gal/LPS and control groups. COX inhibitors reduced the expression of TNF-α mRNA and the activity of NF-κB which were elevated by Gal/LPS treatment. We conclude that COX inhibitors protected the liver from Gal/LPS-induced hepatotoxicity. COX inhibitors could be considered as potential agents in the prevention of acute liver failure and sepsis. © 2011 Elsevier Ltd.en_US
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/foodchemtoxen_US
dc.relation.ispartofFood and Chemical Toxicologyen_US
dc.subjectAcute Liver Injuryen_US
dc.subjectCyclooxygenase Inhibitoren_US
dc.subjectLipopolysaccharideen_US
dc.subjectOxidative Stressen_US
dc.titleCyclooxygenase inhibitors protect d-galactosamine/lipopolysaccharide induced acute hepatic injury in experimental mice modelen_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.doi10.1016/j.fct.2011.11.009en_US
dc.identifier.pmid22107987-
dc.identifier.scopuseid_2-s2.0-84856422951en_US
dc.identifier.hkuros199907-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84856422951&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume50en_US
dc.identifier.issue3-4en_US
dc.identifier.spage861en_US
dc.identifier.epage866en_US
dc.identifier.isiWOS:000303284600062-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLiong, EC=6602732210en_US
dc.identifier.scopusauthoridXiao, J=54942011600en_US
dc.identifier.scopusauthoridLau, TYH=26323763000en_US
dc.identifier.scopusauthoridNanji, AA=54942424200en_US
dc.identifier.scopusauthoridTipoe, GL=7003550610en_US
dc.identifier.citeulike10055250-

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