简介：ThepresentstudywasdesignedtoevaluatetheprotectiveeffectsofethanolextractsofRabdosiajaponicavar.glaucocalyx(Maxim.)Hara(RJ)onlipopolysaccharide(LPS)-inducedacutelunginjury(ALI)inmiceandthepossibleunderlyingmechanismsofaction.ThemicewereorallyadministratedwithRJextract(16,32or64mg?kg–1)dailyforconsecutive7daysbeforeLPSchallenge.Theungspecimensandthebronchoalveolarlavagefluid(BALF)werecollectedforhistopathologicalexaminationsandbiochemicalanalyses.PretreatmentwithRJsignificantlyenhancedsuperoxidedismutase(SOD)activityandreducedthewet-to-dryweight(W/D)ratio,thelevelsofnitricoxide(NO)andproteinleakage,andmyeloperoxidase(MPO)activityinmicewithALI,inadose-dependentmanner.RJreducedcomplementdepositionandsignificantlyattenuatedLPS-inducedALIbyreducingproductionsofinflammatorymediators,suchastumornecrosisfactor-α(TNF-α),interleukin-6(IL-6),andinterleukin-1β(IL-1β).TheresultsdemonstratedthatRJmayattenuateLPS-inducedALIviareducingtheproductionofpro-inflammatorymediators,andreducingcomplementdepositionandradicals.

简介：Thepresentstudywasdesignedtosynthesize2-Cyano-3,12-dioxooleana-1,9(11)-en-28-oate-13β,28-olide(1),alactonederivativeofoleanolicacid(OA)andevaluateitsanti-inflammatoryactivity.Compound1significantlydiminishednitricoxide(NO)productionanddown-regulatedthemRNAexpressionofiNOS,COX-2,IL-6,IL-1β,andTNF-αinlipopolysaccharide(LPS)-stimulatedRAW264.7cells.FurtherinvivostudiesinmurinemodelofLPS-inducedacutelunginjury(ALI)showedthat1possessedmorepotentprotectiveeffectsthanthewell-knownanti-inflammatorydrugdexamethasonebyinhibitingmyeloperoxidase(MPO)activity,reducingtotalcellsandneutrophils,andsuppressinginflammatorycytokinesexpression,andthusamelioratingthehistopathologicalconditionsoftheinjuredlungtissue.Inconclusion,compound1couldbedevelopedasapromisinganti-inflammatoryagentforinterventionofLPS-inducedALI.