Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/68377
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dc.contributor.authorWang, Y.H.en_US
dc.contributor.authorShen, Y.C.en_US
dc.contributor.authorLiao, J.F.en_US
dc.contributor.authorLi, C.H.en_US
dc.contributor.authorChou, C.Y.en_US
dc.contributor.authorLiou, K.T.en_US
dc.contributor.authorChou, Y.C.en_US
dc.date2008zh_TW
dc.date.accessioned2014-06-11T05:56:43Z-
dc.date.available2014-06-11T05:56:43Z-
dc.identifier.issn0007-1188zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/68377-
dc.description.abstractBackground and purpose: Dimemorfan (a sigma(1) receptor agonist) showed neuroprotective properties in animal models of inflammation-mediated neurodegenerative conditions, but its effects on inflammatory cells and systemic inflammation remain unclear. Experimental approach: The effects of dimemorfan on phorbol-12-myristate-13-acetate (PMA)- and N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced neutrophils and lipopolysaccharide (LPS)-activated microglial cells, as well as LPSinduced endotoxin shock in mice were elucidated. Key results: Dimemorfan decreased PMA- and fMLP-induced production of reactive oxygen species (ROS) and CD11b expression in neutrophils, through mechanisms independent of s1 receptors, possibly by blocking ROS production and G-protein-mediated intracellular calcium increase. Dimemorfan also inhibited LPS-induced ROS and nitric oxide (NO) production, as well as that of monocyte chemoattractant protein-1 and tumour necrosis factor-alpha (TNF-alpha), by inhibition of NADPH oxidase (NOX) activity and suppression of iNOS up-regulation through interfering with nuclear factor kappa-B (NF-kappa B) signalling in microglial cells. Treatment in vivo with dimemorfan (1 and 5 mg kg(-1), i.p., at three successive times after LPS) decreased plasma TNF-alpha, and neutrophil infiltration and oxidative stress in the lung and liver. Conclusions and implications: Our results suggest that dimemorfan acts via s1 receptor-independent mechanisms to modulate intracellular calcium increase, NOX activity, and NF-kappa B signalling, resulting in inhibition of iNOS expression and NO production, and production of pro-inflammatory cytokines. These effects may contribute its anti-inflammatory action and protective effects against endotoxin shock in mice.en_US
dc.language.isoen_USzh_TW
dc.relationBritish Journal of Pharmacologyen_US
dc.relation.ispartofseriesBritish Journal of Pharmacology, Volume 154, Issue 6, Page(s) 1327-1338.en_US
dc.relation.urihttp://dx.doi.org/10.1038/bjp.2008.202en_US
dc.subjectcytokineen_US
dc.subjectdimemorfanen_US
dc.subjectendotoxin shocken_US
dc.subjectiNOSen_US
dc.subjectmicroglial cellsen_US
dc.subjectneutrophilsen_US
dc.subjectNF-kappa Ben_US
dc.subjectNOen_US
dc.subjectROSen_US
dc.subjectnitric-oxide synthaseen_US
dc.subjectfactor-kappa-ben_US
dc.subjectoxygen species productionen_US
dc.subjectbv-2en_US
dc.subjectmicroglial cellsen_US
dc.subjecthuman neutrophilsen_US
dc.subjectgene-expressionen_US
dc.subjectantitussiveen_US
dc.subjectactivityen_US
dc.subjectradical productionen_US
dc.subjectsigma-1 receptoren_US
dc.subjecthuman-leukocytesen_US
dc.titleAnti-inflammatory effects of dimemorfan on inflammatory cells and LPS-induced endotoxin shock in miceen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1038/bjp.2008.202zh_TW
item.languageiso639-1en_US-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextno fulltext-
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