Astragalin attenuates lipopolysaccharide-induced inflammatory responses by down-regulating NF-κB signaling pathway

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1、BiochemicalandBiophysicalResearchCommunications419(2012)256–261ContentslistsavailableatSciVerseScienceDirectBiochemicalandBiophysicalResearchCommunicationsjournalhomepage:www.elsevier.com/locate/ybbrcAstragalinattenuateslipopolysaccharide-inducedinflammatoryresponse

2、sbydown-regulatingNF-jBsignalingpathwayaabaaaLananWassySoromou,NaChen,LanxiangJiang,MeixiaHuo,MiaomiaoWei,XiaoChu,cac,⇑a,⇑FayaMartinMillimouno,HaihuaFeng,YoussoufSidime,XumingDengaDepartmentofVeterinaryPharmacology,CollegeofAnimalScienceandVeterinaryMedicine,JilinU

3、niversity,Changchun,Jilin130062,People’sRepublicofChinabDepartmentofDermatology,SecondHospitalofJilinUniversity,Changchun,Jilin130041,People’sRepublicofChinacDepartmentofVeterinaryMedicine,InstituteofScienceandVeterinaryMedicine,Dalaba09,RepublicofGuineaarticleinfo

4、abstractArticlehistory:Astragalin(AG),aflavonoidfrommanytraditionalherbsandmedicinalplants,hasbeendescribedtoReceived29January2012exhibitinvitroanti-inflammatoryactivity.ThepresentstudyaimedtodeterminetheprotectiveeffectsAvailableonline10February2012andtheunderlyingm

5、echanismsofastragalinonlipopolysaccharide-inducedendotoxemiaandlunginjuryinmice.Micewereinjectedintraperitoneally(i.p.)withlipopolysaccharide(LPS)(doserange:5–Keywords:40mg/kg).Weobservedmiceonmortalityfor7daystwiceadayandrecordedsurvivalrates.IndrugAstragalintesti

6、ng,weexaminedthetherapeuticeffectsofastragalin(25,50or75mg/kg)onLPS-inducedendotox-Lipopolysaccharideemiabydosingorallyastragalin1hourbeforeLPSchallenge.UsinganexperimentalmodelofLPS-Inflammatoryresponsesinducedacutelunginjury(ALI),weexaminedtheeffectofastragalininr

7、esolvinglunginjury.Theinves-CytokineEndotoxemiatigationsrevealedthatpretreatmentwithastragalincanimprovesurvivalduringlethalendotoxemiaandAcutelunginjuryattenuateinflammatoryresponsesinamurinemodeloflipopolysaccharide-inducedacutelunginjury.ThemechanismsbywhichAstra

8、galinexertsitsanti-inflammatoryeffectarecorrelatedwithinhibitionoftumornecrosisfactor-a(TNF-a),interleukin-1(IL-1),andinterleukin-6(IL-6)productio