简介:Notopterygiumincisum(QH)hasbeenusedforthetreatmentofrheumatoidarthritis(RA),andvolatileoilsmaybeitsmainlybioactiveconstituents.ThepresentstudywasdesignedtoanalyzethevolatilecompoundsinQHandtodeterminetheanti-arthriticcapacityofNotopterygiumvolatileoilsandthepotentialmechanismofaction.ThevolatilecompoundsanalysiswasconductedbyGC-MS.Theanti-arthriticcapacitytestofthevolatileoilswasconductedonadjuvant-inducedarthritis(AIA)rats.Theanti-inflammatorypropertywastestedinNOreleasemodelinRAW264.7cells.Endothelialcellswereusedtoevaluatetheanti-proliferativeandanti-tubeformativeeffects.70compoundswereanalyzedbyGC-MSinthevolatileoils.NotopterygiumvolatileoilsweakenedtheratAIAinadose-dependentmanner(2,4,and8gcrudedrug/kg).TheNOproductionbyRAW264.7wasdecreasedbymorethan50%inNotopterygiumvolatileoils(5,15,and45μg·mL-1)pretreatedgroups.NotopterygiumvolatileoilsalsoinhibitedEAhy926cellproliferationandfurtherdelayedEAhy926cellcapillarytubeformationinaconcentration-dependentmanner.Theanti-NOproductive,anti-proliferative,andanti-tubeformativeeffectsofNotopterygiumvolatileoilsstronglysuggestedthatthetherapeuticeffectofQHinAIAmightberelatedtothepotentanti-inflammatoryandanti-angiogeniccapacitiesofthevolatileoils.
简介:Carbon-containingrefiactoriesareeasilyoxidizedathightenperature,thusmakingserviceliferapidlydrop.Theanti-oxidationmethods,suchasimpregnationandaddinganti-oxidatonagents,can'tmeettherequire-mentsofindustry'sdevelopmentandsomespecialcases,Byanalyzingthecharcteristicsofseveraloxidesandnon-oxidesrawmaerials,theoxidationresistantmechanismoftherefractoryanti-oxidationcoatings(RAOC),whichpossessthecharacteristcofself-healingathighttemperature,isdiscussed.
简介:ByusingthegeneralizedPoincaréindextheoremitisprovedthatifthen^2criticalpointsofann-polynomialsystemformaconfigurationoftype(2n-1)-(2n-3)+(2n-5)-…+(-1)^n-1,andthe2n-1outmostanti-saddlesformtheverticesofaconvex(2n-1)-polygon,thenamongthese2n-1anti-saddlesatleastonemustbeanode.
简介:Thepresentstudywasdesignedtoexaminetheanti-hyperuricemicandanti-inflammatoryeffectsandpossiblemechanismsofvaticaffinol,aresveratroltetramerisolatedfromethanolextractsofDipterocarpusalatus,inoxonate-inducedhyperuricemicmice.At1hafter250mg·kg~(-1)potassiumoxonatewasgiven,vaticaffinolat20,40,and60mg·kg~(-1)wasintragastricallyadministeredtohyperuricemicmiceoncedailyforsevenconsecutivedays.Vaticaffinolsignificantlydecreasedserumuricacidlevelsandimprovedkidneyfunctioninhyperuricemicmice.Itinhibitedhepaticactivityofxanthinedehydrogenase(XDH)andxanthineoxidase(XOD),regulatedrenalmRNAandproteinlevelsofuratetransporter1(URAT1),glucosetransporter9(GLUT9),organicaniontransporter1(OAT1),organiccationtransporter1(OCT1),OCT2,organiccation/carnitinetransporter1(OCTN1),andOCTN2inhyperuricemicmice.Moreover,vaticaffinolmarkedlydown-regulatedrenalproteinlevelsofNOD-likereceptor3(NLRP3),apoptosis-associatedspeck-like(ASC),andCaspase-1,resultinginthereductionofinterleukin(IL)-1β,IL-18,IL-6andtumornecrosisfactor-α(TNF-α)levelsinthisanimalmodel.Additionally,HPLCandLC-MSanalysesclearlytestifiedthepresenceofvaticaffinolinthecrudeextract.Theseresultssuggestthatvaticaffinolmaybeusefulforthepreventionandtreatmentofhyperuricemiawithkidneyinflammation.
简介:China'sAnti-JapaneseWarWORLDWARⅡ,whichendedhalfacenturyagoinacrushingdefeatforthefascistpowers,wasalife-and-deathstrugglebetw...
简介:Anti-globalizationtrendsareinplayintheUSandWesternEuropewhereelectoratesarerecalcitranttoallowimmigrantsintotheirsocieties,nationalsovereigntyissoughtincertaingeographicareas,andthenationalmoodseekstosuppressnewlyrisingcountries'tradeanddevelopment.ThecontinuationofeconomicdownturninWesterncountriesisreinforcedbytheirinternalwealthgapandexternalcompetition.Ascapitalism'sdemandforprofitisnowbeingcritiquedalongwiththeemergentprofitprospectstobedeliveredbypendingtechnologicalprogress,thetemperofthetimescouldtemporarilyslowdownbutnotreverseglobalization.Timelydiscussionsaboutreformofinternationaleconomicorderandaboutaneffectivenationaldevelopmentmodelshouldseeksustainablesolutionsforhealthy,stableglobalizationanddevelopmentoftheworldeconomy.
简介:Therearefewstudiesontheneuroprotectiveeffectsofsyringaldehydeinaratmodelofcerebralischemia.Thestudyaimedtoelucidatethemechanismsunderlyingtheneuroprotectiveeffectsofsyringaldehydeonischemicbraincells.Ratmodelsofcerebralischemiawereintraperitoneallyadministeredsyringaldehyde.At6and24hoursaftersyringaldehydeadministration,celldamageinthebrainofcerebralischemiaratswasobviouslyreduced,superoxidedismutaseactivityandnuclearrespiratoryfactor1expressioninthebraintissueweremarkedlyincreased,malondiadehydelevelwasobviouslydecreased,apoptosis-relatedcysteinepeptidasecaspase-3and-9immunoreactivitywasobviouslydecreased,andneurologicalfunctionwasmarkedlyimproved.Thesefindingssuggestthatsyringaldehydeexertsneuroprotectiveeffectsoncerebralischemiainjurythroughanti-oxidationandanti-apoptosis.