File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)

Conference Paper: Nitric oxide in an acute liver injury model

TitleNitric oxide in an acute liver injury model
Authors
Issue Date2005
PublisherLongman
Citation
The 187th Meeting of the Pathological Society of Great Britain and Ireland, London, UK, 6–7 January 2005. In Journal of Pathology, 2005, v. 205 n. S1, p. A11 How to Cite?
AbstractWe investigated whether a high level of nitric oxide (NO) is protective or injurious in acute liver injury. An acute phase ICR mice model was used by injecting CC1, with or without NO inhibitors (SMT and L-NIL) and NO donor (SNP). Blood and liver tissues were collected. Immunocytochemistry, RT-PCR, Western Blotting, EMSA, semm ALT and total 8-isoprostane analyses were performed. Our results showed high levels of ALT with liver cells necrosis, increased total 8-isoprostane and nitrotyrosine protein after CC4 administration. NO inhibitors and SNP abrogated these effects. Protein and mRNA levels in CCL-treated mice demonstrated upregulation of TNF-a, iNOS, and COX-2. NO inhibitors with CC4 diminished the expression of these proinflammatory mediators. NF-KB was also upregulated in CC4 treated mice but was reversed in NO inhibitors pretreated mice. CCl4 with SNP showed slightly lower expression of COX-2 when compared with CC14 treated mice but not for TNF-a, iNOS and NF-KB activity. Partial protection of SNP from lipid peroxidation and oxidative stress is due to its scavenging action. We conclude that high level of NO is detrimental in acute liver injury and can he ameliorated by decreasing the NO level with NO inhibitors and NO donor.
Persistent Identifierhttp://hdl.handle.net/10722/95741
ISSN
2015 Impact Factor: 7.381
2015 SCImago Journal Rankings: 4.176

 

DC FieldValueLanguage
dc.contributor.authorLeung, TMen_HK
dc.contributor.authorTipoe, GLen_HK
dc.contributor.authorLau, THYen_HK
dc.contributor.authorLiong, ECen_HK
dc.contributor.authorSo, Hen_HK
dc.contributor.authorLeung, KMen_HK
dc.contributor.authorLeung, WMen_HK
dc.contributor.authorTom, WMen_HK
dc.contributor.authorFung, MLen_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorNanji, AAen_HK
dc.date.accessioned2010-09-25T16:11:47Z-
dc.date.available2010-09-25T16:11:47Z-
dc.date.issued2005en_HK
dc.identifier.citationThe 187th Meeting of the Pathological Society of Great Britain and Ireland, London, UK, 6–7 January 2005. In Journal of Pathology, 2005, v. 205 n. S1, p. A11en_HK
dc.identifier.issn0022-3417-
dc.identifier.urihttp://hdl.handle.net/10722/95741-
dc.description.abstractWe investigated whether a high level of nitric oxide (NO) is protective or injurious in acute liver injury. An acute phase ICR mice model was used by injecting CC1, with or without NO inhibitors (SMT and L-NIL) and NO donor (SNP). Blood and liver tissues were collected. Immunocytochemistry, RT-PCR, Western Blotting, EMSA, semm ALT and total 8-isoprostane analyses were performed. Our results showed high levels of ALT with liver cells necrosis, increased total 8-isoprostane and nitrotyrosine protein after CC4 administration. NO inhibitors and SNP abrogated these effects. Protein and mRNA levels in CCL-treated mice demonstrated upregulation of TNF-a, iNOS, and COX-2. NO inhibitors with CC4 diminished the expression of these proinflammatory mediators. NF-KB was also upregulated in CC4 treated mice but was reversed in NO inhibitors pretreated mice. CCl4 with SNP showed slightly lower expression of COX-2 when compared with CC14 treated mice but not for TNF-a, iNOS and NF-KB activity. Partial protection of SNP from lipid peroxidation and oxidative stress is due to its scavenging action. We conclude that high level of NO is detrimental in acute liver injury and can he ameliorated by decreasing the NO level with NO inhibitors and NO donor.-
dc.languageengen_HK
dc.publisherLongman-
dc.relation.ispartofJournal of Pathologyen_HK
dc.titleNitric oxide in an acute liver injury modelen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailTipoe, GL: tgeorge@hkucc.hku.hken_HK
dc.identifier.emailLiong, EC: eclionga@HKUCC.hku.hken_HK
dc.identifier.emailTom, WM: wmtoma@hkucc.hku.hken_HK
dc.identifier.emailFung, ML: fungml@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityTipoe, GL=rp00371en_HK
dc.identifier.authorityTom, WM=rp00237en_HK
dc.identifier.authorityFung, ML=rp00433en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/path.1712050102-
dc.identifier.hkuros104823en_HK
dc.identifier.volume205en_HK
dc.identifier.spage11en_HK
dc.identifier.epage11en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats