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Dimemorfan also inhibited LPS\u2010induced ROS and nitric oxide (NO) production, as well as that of monocyte chemoattractant protein\u20101 and tumour necrosis factor\u2010alpha (TNF\u2010\u03b1), by inhibition of NADPH oxidase (NOX) activity and suppression of iNOS up\u2010regulation through interfering with nuclear factor kappa\u2010B (NF\u2010\u03baB) signalling in microglial cells. Treatment <jats:italic>in vivo<\/jats:italic> with dimemorfan (1 and 5\u2003mg\u2003kg<jats:sup>\u22121<\/jats:sup>, i.p., at three successive times after LPS) decreased plasma TNF\u2010\u03b1, and neutrophil infiltration and oxidative stress in the lung and liver.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and implications:<\/jats:title><jats:p>Our results suggest that dimemorfan acts <jats:italic>via<\/jats:italic> \u03c3<jats:sub>1<\/jats:sub> receptor\u2010independent mechanisms to modulate intracellular calcium increase, NOX activity, and NF\u2010\u03baB signalling, resulting in inhibition of iNOS expression and NO production, and production of pro\u2010inflammatory cytokines. These effects may contribute its anti\u2010inflammatory action and protective effects against endotoxin shock in mice.<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2008) <jats:bold>154<\/jats:bold>, 1327\u20131338; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/bjp.2008.202\">10.1038\/bjp.2008.202<\/jats:ext-link>; published online 26 May 2008<\/jats:p><\/jats:sec>","DOI":"10.1038\/bjp.2008.202","type":"journal-article","created":{"date-parts":[[2008,5,26]],"date-time":"2008-05-26T10:16:25Z","timestamp":1211796985000},"page":"1327-1338","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Anti\u2010inflammatory effects of dimemorfan on inflammatory cells and LPS\u2010induced endotoxin shock in 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