糖基化末端終產(chǎn)物脂質(zhì)過(guò)氧化

ElsevierTermOne:AdvancedglycationendElsevierTermOne:Advancedglycationendproducts(2013年至今共檢索到34篇相關(guān)文獻(xiàn)1.SulforaphanereducesadvancedglycationendproductsinducedinflammationinendothelialcellsandrataortaNutrition,MetabolismandCardiovascularDiseases,InPress,Manuscript,Availableonline21April2016TakanoriMatsui,NobutakaNakamura,AyakoOjima,YuriNishino,Sho-ichiBackgroundandAdvancedglycationendproducts(AGEs)-thereceptorRAGEinteractionevokesoxidativestressandinflammatoryreactions,therebybeinginvolvedinendothelialcell(EC)damageindiabetes.Sulforaphaneisgeneratedfromglucoraphanin,anaturallyoccurringisothiocyanatefoundinwidelyconsumedcruciferousvegetables,bymyrosinase.Sulforaphanehasbeenreportedtoprotectagainstoxidativestress-mediatedcellandtissueinjury.However,effectsofsulforaphaneonAGEs-inducedvasculardamageremainMethodsandInthisstudy,weinvestigatedwhetherandhowsulforaphanecouldinhibitinflammationinAGEs-exposedhumanumbilicalveinECs(HUVECs)andAGEs-injectedrataorta.Sulforaphanetreatmentfor4or24hdose-dependentlyinhibitedtheAGEs-inducedincreaseinRAGE,monocytechemoattractantprotein-1(MCP-1),intercellularadhesionmolecule-1(ICAM-1),andvascularcelladhesionmolecular-1(VCAM-1)geneexpressioninHUVECs.AGEssignificantlystimulatedMCP-1productionby,andTHP-1celladhesionto,HUVECs,bothofwhichwerepreventedby1.6μMsulforaphane.SulforaphanesignificantlysuppressedoxidativestressgenerationandNADPHoxidaseactivationevokedbyAGEsinHUVECs.Furthermore,aorticRAGE,ICAM-1andVCAM-1expressioninAGEs-injectedratswereincreased,whichweresuppressedbysimultaneousinfusionofThepresentstudydemonstratedforthefirsttimethatsulforaphanecouldinhibitinflammationinAGEs-exposedHUVECsandAGEs-infusedrataortapartlybysuppressingRAGEexpressionthroughitsanti-oxidativeproperties.InhibitionofThepresentstudydemonstratedforthefirsttimethatsulforaphanecouldinhibitinflammationinAGEs-exposedHUVECsandAGEs-infusedrataortapartlybysuppressingRAGEexpressionthroughitsanti-oxidativeproperties.InhibitionoftheAGEs-RAGEaxisbysulforaphanemightbeanoveltherapeutictargetforvascularinjuryin2.Atorvastatinpreventsadvancedglycationendproducts(AGEs)-inducedcardiacfibrosisviaactivatingperoxisomeproliferator-activatedreceptorgamma(PPAR-γ)Metabolism,Volume65,Issue4,April2016,Pages441-MiaoChen,HongweiLi,GuoxingWang,XuhuaShen,ShumeiZhao,WenPreviousstudieshaveshownthattheactivationofadvancedglycationendproducts(AGEs)contributedtothecardiacfibrosisindiabeticpatients.Althoughithadbeenreportedthatstatinshavebeneficialeffectsoncardiacfibrosisinhypertensionandmyocardialischemiamodels,theireffectsonAGEsmodelshavenotbeenstudied.Weaimedtoinvestigatetheeffectsofatorvastatin(Ator)ontheAGEs-inducedcardiacfibrosisbothinvitroandMaleSprague-Dawleyratswererandomlydividedintofourgroups:Control,AGEs,AtororAGEs+Ator.Thecardiacfunctionwasevaluatedwiththeechocardiographyatthesecondandthethirdmonth.Fibrosisarea,α-SMAandRAGEexpressionincardiactissueweremeasured.Forinvitrostudy,ratcardiacfibroblastsweretreatedwithPD98059(ERKinhibitor),AtororAtor+GW9662(PPAR-γantagonist),andthenwerestimulatedwithAGEs.Fibroblastsproliferation,ERK1/2,phosphorylatedERK1/2,α-SMA,andRAGEexpressionwereComparedwiththecontrolgroup,invivotreatmentwithAtorsignificantlyretardedtheAGEs-induceddiastolicfunctionandattenuatedcardiacfibrosis,α-SMA,andRAGEoverexpressioninducedbyAGEs.Consistently,AtorprominentlydownregulatedRAGEandα-SMA,whileinhibitedphosphorylationofERK1/2andfibroblastproliferationinducedbyAGEsinvitro.TheGW9662neutralizedtheseeffectsofAtoroncardiacfibroblastsstimulatedbyInthisstudy,wedemonstratedthatAGEs-inducedfibroblastproliferationanddifferentiationweredependentonAGEs-RAGE-ERK1/2pathwayandthatatorvastatincouldblockthispathwayviaactivating3.Dietaryadvancedglycationendproducts(AGEs)3.Dietaryadvancedglycationendproducts(AGEs)inducechronickidneydisease(CKD)andchangesinguthomeostasisJournalofNutrition&IntermediaryMetabolism,Volume4,June2016,PageBackground/Aims:Ulcerativecolitis(UC),atypeofinflammatorydisease,ischaracterisedbycolonicinflammationandulceration.OrallyadministeredEmuOil(EO),extractedfromEmufat,acceleratedtheintestinalrepairprocessinapre-clinicalmodelofacuteUC.WehypothesizedthatEOwouldreducetheseverityofdextransulphatesodium(DSS)-inducedchronicUCinMethods:FemaleC57BL/6mice(n?10/group)weregavagedwithwaterorEO(80mLor160mL)thriceweekly.MiceweresubjectedtotwocycleseachconsistingofadlibitumaccesstowaterorDSS(2%w/v)foroneweekandtwoweekswaterrecovery.FollowedbyoneweekwaterorDSSandmiceculledtwodayslater.Bodyweight,bloodprofile,organdataandmyeloperoxidaseactivitywereassessed.p<0.05wasconsideredResults:DSSdecreasedbodyweight(days6-19and26-30;maximumof24%),comparedtonormalcontrols(p<0.001).InDSS-treatedmice,highdoseEOsignificantlyincreasedbodyweight(days6-12),comparedtocontrols(p<0.05).DSSdecreasedredbloodcellcount,comparedtonormalcontrols(p<0.05);aneffectnotimprovedbyEO.Comparedtonormalcontrols,DSSincreasedliver(16%),spleen(45%),lung(19%)andsmallintestine(20%)weights(p<0.05),althoughEOhadnosignificanteffect(p>0.05).DSSincreasedcolonmyeloperoxidaseactivitycomparedtonormalcontrols(p<0.05),however,EOwasunabletosignificantlyreducetheseConclusions:EOpreventedbodyweightlossinthismousemodelofchroniccolitis,however,wasunabletoimproveotherpreliminaryparameters.Analysescurrentlyunderwayincludechronicmarkers,histologicalmorphometryandcell4.Measurementofurinaryadvancedglycationend-products(AGEs)usingafluorescenceassayformetabolicsyndrome-relatedscreeningtestsDiabetes&MetabolicSyndrome:ClinicalResearch&Reviews,InPress,CorrectedProof,Availableonline12November2015AkiraSuehiro,KagehiroUchida,MamoruNakanishi,IchiroThesimplescreeningtestofadvancedglycationend-products(AGEs)hasnotbeenestablishedyet.aimedtoclarifytheusefulnessofsimplemeasurementofAGEsforscreeningThesubjectswerehealthyThesubjectswerehealthyparticipantsandpatientswithmetabolicsyndrome.Urinesamplesweredilutedfrom1:10to1:200usingphosphate-bufferedsaline,andthefluorescenceintensitywasmeasuredat440nmafterexcitationat370nmina96-wellmicroplatespectrophotometer.TheobtainedintensitieswereadjustedaccordingtotheurinarycreatinineInpatientswithmetabolicsyndrome,urinaryAGElevelsweresignificantlyhigherthaninhealthyindividuals(median[range],168.25[82.51–1276.15]AU/gcreatinine[n=37]versus134.67[37.86–776.31]AU/gcreatinine[n=350],respectively;p=0.0066).WefoundsignificantpositivecorrelationsbetweenurinaryAGEsandsystolicanddiastolicbloodpressures(Spearman'scorrelationr=0.119[p=0.019]andr=0.128[p=0.012],respectively).TherewasnosignificantcorrelationbetweenestimatedglomerularfiltrationrateandurinaryAGEs(r=0.018[p=0.744]),confirmingthatrenaldysfunctiondidnotinfluenceresultsofurinaryAGEmeasurements.Whenalloftheparticipantsinthestudywereclassifiedintofourgroupsaccordingtothenumbersofcomponentsofmetabolicsyndrome,wefoundasignificanttendency(p=0.0127)forurinaryAGElevelstobehigherwiththeincreasingnumberofmetabolicsyndromeTheseresultssuggestedthatmeasurementofurinaryAGElevelsmaybeusefulforevaluatingtheriskmetabolic5.SuppressionofantioxidantNrf-2anddownstreampathwayinH9c2cellsbyadvancedglycationendproducts(AGEs)viaERKphosphorylationBiochimie,Volume118,November2015,Pages8-Shun-YaoKo,Shu-ShingChang,I-HsuanLin,Hong-IDiabeticcardiomyopathyisrelatedtooxidativestressandcorrelatedwiththepresenceofadvancedglycationendproducts(AGEs).Inaclinicalsetting,AGEscanbedetectedinpatientspresentingdiabeticcardiomyopathy;however,theunderlyingmechanismhasyettobeelucidated.Inourpreviousstudy,AGEsincreasecellhypertrophyviaERKphosphorylationinaprocesscloselyrelatedtoROSproduction.Thus,weproposethatAGEsregulatetheantioxidantgenenuclearfactor-erythroid2-relatedfactor(Nrf-2).InH9c2cellstreatedwithAGEs,theexpressionofNrf-2wasreduced;however,ERKphosphorylationwasshowntoincrease.TreatmentwithH2O2wasalsoshowntoincreaseNrf-2andERKphosphorylation.IncellspretreatmentwithROSscavengerNAC,theeffectsofH2O2werereduced;however,theeffectsoftheAGEsremainedlargelyunchanged.Conversely,whencellswerepretreatedwithPD98059(ERKinhibitor),theexpressionofNrf-2wasrecoveredfollowingtreatmentwithAGEs.OurresultssuggestthatAGEsinhibitNrf-2viatheERKpathway;however,thisinfluenceispartlyassociatedwithROS.OurfindingfurtherindicatedthatAGEspossessbothROS-dependentandROS-independentpathways,resultinginareductioninNrf-2.Thisreportrevealsanimportantmechanismunderlyingtheregulationofdiabetic6.Fluorophoresadvancedglycationendproducts(AGEs)-to-NADHratioispredictorfordiabeticchronickidneyandcardiovasculardiseaseJournalofDiabetesanditsComplications,Volume29,JournalofDiabetesanditsComplications,Volume29,Issue7,September–October2015,Pages893-897DanaM.Ciobanu,LoredanaE.Olar,RazvanStefan,IoanA.Veresiu,G.Bala,PetruA.Mircea,GabrielaAnimbalanceinadvancedglycationendproducts(AGEs)andNADHformationhasbeenassociatedwithdiabeticchronickidneydisease(CKD)andcardiovasculardisease(CVD).NodatahavebeenreportedonsimultaneousmeasurementofAGEsandNADHintype2diabetes(T2DM)patients.WeaimedtocompareAGEs,NADHandtheAGEs-to-NADHratioinT2DMandcontrols,andtoassessitsrelationshipwithdiabeticCKDandMaterialandInthiscross-sectionalstudy,wemeasuredserumAGEs(370/435nm)andNADH(370/460nm)inT2DMpatients(n=63)andcontrols(n=25)usingfluorescencespectroscopy.TheAGEs-to-NADHratioanalyzedaccordingtodiabeticCKDandWefoundsignificantlyhigherAGEs-to-NADHratioinT2DMcomparedtocontrols.TheAGEs-to-NADHratiowassignificantlyassociatedwithtriglycerides,bloodglucose,HDL-cholesterol,estimatedglomerularfiltrationrate.TheAGEs-to-NADHratiowasasignificantpredictorforthepresenceofdiabeticCKDandCVDwhenusingROCcurves.MultivariateanalysisshowedthattriglyceridesandthepresenceofT2DMwerepredictorsfortheAGEs-to-NADHThesefindingssuggestthatthefluorophoresAGEs-to-NADHratiocouldbeanewbiomarkerforpresenceofdiabeticCKDand7.Inhibitionandbreakingofadvancedglycationend-products(AGEs)withbis-2-aminoimidazolederivativesTetrahedronLetters,Volume56,Issue23,3June2015,Pages3406-MikeA.Richardson,RobertE.Furlani,BrendanK.Podell,DavidF.Ackart,JessicaD.Haugen,RobertaJ.Melander,ChristianMelander,RandallJ.Advancedglycationend-products(AGEs),unregulatedmodificationstohostmacromoleculesthatoccurasaresultofmetabolicdysregulation,playaroleinmanydiabetesrelatedcomplications,inflammationandaging,andmayleadtoincreasedcardiovascularrisk.SmallmoleculesthathavetheabilitytoinhibitAGEformation,andevenbreakpreformedAGEshaveenormoustherapeuticpotentialinthetreatmentoftheidentificationofabis-2-aminoimidazoleleadcompoundtheidentificationofabis-2-aminoimidazoleleadcompoundthatpossessessuperiorAGEinhibitionbreakingactivitycomparedtotheknownAGEinhibitor8.InhibitoryeffectofpolyphenolsinHouttuyniacordataonadvancedglycationend-products(AGEs)bytrappingmethylglyoxalLWT-FoodScienceandTechnology,Volume61,Issue1,April2015,158-So-RaYoon,Soon-MiTheinhibitoryeffectofbioactivecomponentsfromHouttuyniacordata(H.cordata)onadvancedglycationend-products(AGEs)bytrappingmethylglyoxal(MGO)wasinvestigated.MGOanditsadductsofquercitrin,chlorogenicacid,rutinwasanalyzedbyusingliquidchromatography-massspectrometry(LC-MS/MSn).TheremainingMGOwere52.3,26.7,and9.4%forchlorogenicacid,quercitrin,andrutin,respectivelyandthemono-ordi-MGOconjugatedadductsofquercitrinandrutinwereidentifiedat24hofreaction.TheformationofAGEswasdetectedthroughthereactionofglucosewithproteinbythefluorescencemethod.Duringtheglycationreaction,quercitrin,rutin,andmethanolextractofH.cordatadecreasedtheproductionlevelofAGEsby91–94.6%.H.cordatacontainingchlorogenicacid,quercitrin,andrutinmayhavepotentialroleinminimizingAGEs9.Advancedglycationendproducts(AGEs)andthesolublereceptorAGE(sRAGE)inpatientswithtype1diabetesandcoeliacNutrition,MetabolismandCardiovascularDiseases,Volume25,IssueFebruary2015,Pages230-S.BackgroundandAdvancedglycationend(AGE)productsplayaroleintheprogressionofdiabeticcomplications.Gluten-freediet(GFD)mightaffectAGElevelsinpatientswhoadheretoaGFDbecauseofcoeliacdisease(CD).TheaimofourstudywastocompareskinAGElevelsandsolublereceptorAGElevels(sRAGE)inpatientswithtype1diabetes(T1DM)with(T1DM+CD)andwithoutCD(T1DM–CD)andhealthyMethodsandWerecruited25T1DM+CDand25T1DM–CDpatients,matchedforage,gender,diabetesandglycaemiccontrolalongside25healthycontrols.Wecollecteddemographic,clinicalandbiochemicalcharacteristics,includingskinautofluorescence(AF),sRAGEandhs-CRPlevels.Thedurationofinpatientswas30±inpatientswas30±14(+CD)and29±14years(?CD),whereasCDdurationinT1DM+CDpatientswas1.9±0.4,p<0.01)andskinAFwasindependentlyassociatedwithage(r=0.72,p<0.01).sRAGElevelswerehigherinT1DM–CDpatientscomparedtohealthycontrols(1554±449versus1309±400,p0.049)andindependentlyassociatedwithcreatininelevels(r=0.32,p<OurstudydemonstratesthatskinAGEandsRAGElevelsareelevatedinT1DMpatientscomparedwithhealthycontrols.NodifferenceinskinAForsRAGElevelsbetweenT1DMpatientswithorwithoutCDwereobserved.ThepresentstudysuggeststhatdifferencesinmicrovascularcomplicationsbetweenT1DMandT1DM+CDpatientsarenotduetodifferencesinskinAForsRAGE10.Evaluationoftheinvitroinhibitoryeffectsofbuckwheatenhancedwheatbreadextractsontheformationofadvancedglycationproducts327-DorotaSzawara-Nowak,GeorgiosKoutsidis,Wies?awWiczkowski,Inthisstudy,theinhibitoryeffectsofextractsfrombuckwheatenhancedwheatbreads,ontheformationoffluorescentadvancedglycationend-products(AGEs)werestudiedinbovineserumalbumin(BSA)/glucoseandBSA/methylglyoxal(MGO)systems.Correlationswithtotalphenoliccompounds(TPC),totalflavonoids(TF)aswellasrutin(Ru)andquercetin(Q)contentswerealsoWhitebuckwheatflourorflourfromroastedbuckwheatgroatswasusedtosubstitutewhiteordarkwheatflourat0,10,20,30and50%w/wontotalflourbasis.TheinhibitoryeffectagainstAGEsformationinBSA-glucoseandBSA-MGOsystemsdependedonthelevelofsubstitutionandtypeofflourused.TheextractsfrombuckwheatenhanceddarkwheatbreadsshowedthehighestinhibitoryactivityagainstAGEsformationwhichwasweaklycorrelatedtothephenolicscontent.Incontrast,weakinhibitoryeffectswereobservedforbuckwheatenhancedwhitewheatbreadsandtheseeffectswerehighlycorrelatedwithTPCandTFaswellasRuandQThepotentinhibitionofbuckwheatenhancedbreads,formulatedwithdarkwheatflourandflourfromroastedbuckwheatgroats,againstThepotentinhibitionofbuckwheatenhancedbreads,formulatedwithdarkwheatflourandflourfromroastedbuckwheatgroats,againstAGEsformationsuggesttheirpossiblebeneficialrolesinthe11.Emergingroleofadvancedglycation-endproducts(AGEs)inpathobiologyofeyeProgressinRetinalandEyeResearch,Volume42,September2014,85-StylianosA.Kandarakis,ChristinaPiperi,FotisTopouzis,AthanasiosAdvancedglycationendproducts(AGEs)havebeenimplicatedinvisionlossassociatedwithThispathogenicpotentialismainlyattributedtotheiraccumulationinoculartissueswheretheymediateaberrantcrosslinkingofextracellularmatrixproteinsanddisruptionofendothelialjunctionalcomplexesthataffectscellpermeability,mediatesangiogenesisandbreakdownoftheinnerblood-retinalbarrier.Furthermore,AGEsseverelyaffectcellularmetabolismbydisruptingATPproduction,enhancingoxidativestressandmodulatinggeneexpressionofanti-angiogenicandanti-inflammatorygenes.ElucidationofAGE-inducedmechanismsofactionindifferenteyecompartmentswillhelpintheunderstandingofthecomplexcellularandmolecularprocessesassociatedwitheyediseases.Severalpharmaceuticalagentswithanti-glycatingandanti-oxidantpropertiesaswellasAGEcrosslink‘breakers’havebeencurrentlyappliedtoeyediseases.Theroleofdietandthebeneficialeffectsofcertainnutriceuticalsprovideanalternativewaytomanagechronicvisualdisordersthataffectthequalityoflifeofmillionsof12.AdvancedglycationendproductsacceleratearteriosclerosisrenaltransplantationthroughtheAGE/RAGE/ILKExperimentalandMolecularPathology,Volume99,Issue2,OctoberPages312-XuzhongLiu,KunLiu,ZijieWang,ChaoLiu,ZhijianHan,JunTao,PeiLu,Wang,BianWu,ZhengkaiHuang,ChangjunYin,MinGu,RuoyunTheeffectsofadvancedglycationendproducts(AGEs)onarteriosclerosis(AS)aftertransplantationandthemolecularmechanismsinvolvedremainSampleswerecollectedfrom30healthyvolunteersSampleswerecollectedfrom30healthyvolunteersand30renaltransplantrecipients(RTRs)todeterminethelevelsofAGEsandtoobservebothhistologicalchangesandα-smoothmuscleactin(α-SMA)andosteopontin(OPN)expression.Furthermore,weanalyzedα-SMA,OPNandintegrin-linkedkinase(ILK)inratvascularsmoothmusclecells(VSMCs)thatweretreatedwithAGEsandinILKplasmidtransfectedratVSMCstreatedwithAGEs.Finally,wemeasuredtheexpressionofILKandthereceptorforadvancedglycationend(RAGE)productsinratVSMCstreatedwithAGEsandananti-RAGESignificantdifferencesinthehistologicalchanges,serumAGEs,andexpressionofα-SMAandOPNinarterialwallswerenotedbetweenhealthyvolunteersandRTRs.SignificantOPNandILKoverexpressionandreducedα-SMAexpressionweredetectedinatime-dependentmannerinratVSMCsaftertreatmentwithAGEs.SimilaroutcomeswereobservedregardingtheoverexpressionofILK,andtheseresultscouldbepreventedviaRAGE13.Increasedadvancedglycationend-products(AGEs)assessedbyautofluorescenceinJournalofPsychiatricResearch,Volume47,Issue8,August2013,1044-YoussefKouidrat,AliAmad,RachelDesailloud,MomarDiouf,EvaDaphnéScoury,Jean-DanielLalau,GwenoléOxidativestresshasbeenintensivelystudiedasakeybiochemicalsysteminthepathophysiologyofschizophrenia.However,littleisknownabouttheimplicationofoxidativestressinthedevelopmentofphysicalillnessesinschizophreniapatients,whoarecharacterizedbyhighcardiovascularriskanddecreasedlifeexpectancy.Advancedglycationend-products(AGEs)areconsideredtobemarkersofoxidativestressandarelinkedtothedevelopmentofWeinvestigatedAGElevelsdeterminedbyanoninvasiveskinautofluorescence(skinAF)methodorrenaldiseaseand55orrenaldiseaseand55healthycontrolsmatchedforage,genderandsmokingstatus.Nineteenoftheschizophreniapatientshadasevereformofthedisease(KraepelinianSkinAFwassignificantlyhigherinschizophreniapatientscomparedtocontrols(2.46±0.52and1.90±0.21,respectively,p<0.0001).KraepelinianschizophreniapatientshadsignificantlyhigherskinAF14.UsefulnessofPreproceduralLevelsofAdvancedGlycationEndProductstoPredictRestenosisinPatientsWithControlledDiabetesMellitusUndergoingDrug-ElutingStentImplantationforStableAnginaPectoris(FromtheProspectiveARMYDA-AGEsTheAmericanJournalofCardiology,Volume112,Issue1,1July2013,21-CristianoSpadaccio,GiuseppePatti,FedericoDeMarco,RaffaellaCoccia,FabioDiDomenico,FrancescoPollari,RobertaZanzonico,MatteoMarioLusini,GermanoDiSciascio,ElvioCovino,MassimoDiabetesmellitus(DM)remainsthemainpredictorofrestenosisratesandcardiovasculareventsfollowingsuccessfulpercutaneouscoronaryintervention(PCI)despitetheuseofdrug-elutingstents(DES).HbA1c<6.0%isconsideredanindexofoptimizedmetaboliccontrolinpatientswithDM,butseveralstudiesaredownsizingitsroleintheclinicalmanagementofthesepatients.Increasingevidencepointsattheroleofadvancedglycationendproducts(AGEs)inrestenosispathogenesisindependentlyonHb1AClevels.Thus,weinvestigatedthepredictivevalueofpreproceduralAGElevelsforin-stentrestenosisinapopulationofeuglycaemicdiabeticpatientsundergoingPCIwithDESimplantation.Onehundredtwenty-fiveconsecutivepatientswithDMinoptimizedglycemiccontroladmittedforstableanginapectorisandtreatedwithelectiveDESimplantationatatertiaryhospitalwereprospectivelyincluded.TheprimaryendpointoftheARMYDA-AGEsstudywastocompareratesofangiographicISRat6monthsaftertheinterventionaccordingtopre-PCIlevelsofAGEs.SecondaryendpointswerethecorrelationsofAGElevelswithoccurrenceofperiproceduralmyocardialdamage,majoradversecardiacevents,andin-stentlatelossat6-monthcontrolcoronaryangiography.AGElevels>17μMwasfoundtobeanindependentpredictorofISRat6monthsandstentlumenloss.AGEsfailedtopredictoccurrenceofsecondaryendpoints.Inconclusion,elevatedAGElevelspredictoccurrenceofin-stentrestenosisafterimplantationinpatientswithDMonoptimizedimplantationinpatientswithDMonoptimizedglycemiccontrolandmightrepresentadosablemarkeradverseoutcomeafter15.Serumlevelsofadvancedglycationendproducts(AGEs)areindependentlycorrelatedwithcirculatinglevelsofdipeptidylpeptidase-(DPP-4)inClinicalBiochemistry,Volume46,Issues4–5,March2013,Pages300-NobuhiroTahara,Sho-ichiYamagishi,MasayoshiTakeuchi,AtsukoKumikoKaifu,SeijiUeda,SeiyaOkuda,TsutomuInhibitionofdipeptidylpeptidase-4(DPP-4)hasbeenproposedasapotentialtherapeutictargetfortype2diabetes.AlthoughsolubleDPP-4hasbeenidentifiedinhumanserumandcouldbeassociatedwithDPP-4activity,thekineticsandregulationofcirculatingDPP-4levelsremainunknown.Inthisstudy,weexaminedwhichanthropometricandmetabolicvariables,includingserumlevelsofadvancedglycationendproducts(AGEs),wereindependentlyassociatedwithserumDPP-4levels.Further,weinvestigatedtheeffectsofAGEsonDPP-4expressionin,andsolubleDPP-4releasefromhumanculturedDesignandThestudyinvolved432consecutiveoutpatients(301malesand131females;meanages61.8±8.8)whounderwentcompletehistoryandphysicalexaminations,anddeterminationsofbloodchemistryandanthropometricvariables.SerumDPP-4andAGElevelswereexaminedbyenzyme-linkedimmunosorbentassay.ProteinexpressionlevelsofDPP-4anditsreleasefromthecellswereanalyzedwithwesternblotMeanserumlevelsofDPP-4andAGEswere520.2±39.9ng/mLand8.96±2.57U/mL,respectively.Inmultipleregressionanalysis,female(p<0.001),HDL-cholesterol(p<0.001),glycatedhemoglobin(p<0.001),AGEs(p<0.03),andtheabsenceofhypertensionmedication(p<0.05)areindependentlyassociatedwithDPP-4levels(R2=0.167).WesternblotanalysisrevealedthatAGEssignificantlyincreasedDPP-4expressionin,andsolubleDPP-4releasefromtubularparametersinageneralpopulation.AGEsmayup-regulatecellularDPP-4expressionandsubsequentlyincreasecirculatinglevelsofDPP-4inhumans.16.Fibroblastgrowthfactor21protects16.Fibroblastgrowthfactor21protectsmousebrainagainstd-galactoseinducedagingviasuppressionofoxidativestressresponseadvancedglycationendproductsPharmacologyBiochemistryandBehavior,Volume133,June2015,122-YinhangYu,FuliangBai,WenfeiWang,YaonanLiu,QingyanYuan,SusuTongZhang,GuiyouTian,SimingLi,DeshanLi,GuipingFibroblastgrowthfactor21(FGF21)isahormonesecretedpredominantlyintheliver,pancreasandadiposetissue.Recently,ithasbeenreportedthatFGF21-Transgenicmicecanextendtheirlifespancomparedwithwildtypecounterparts.Thus,wehypothesizethatFGF21mayplaysomerolesinagingoforganisms.Inthisstudyd-galactose(d-gal)-inducedagingmicewereusedtostudythemechanismthatFGF21protectsmicefromaging.Thethree-month-oldKunmingmiceweresubcutaneouslyinjectedwithd-gal(180mg·kg?1·d?1)for8weeksandadministeredsimultaneouslywithFGF21(1,2or5mg·kg?1·d?1).OurresultsshowedthatadministrationofFGF21significantlyimprovedbehavioralperformanceofd-gal-treatedmiceinwatermazetaskandstep-downtest,reducedbraincelldamageinthehippocampus,andattenuatedthed-gal-inducedproductionofMDA,ROSandadvancedglycationendproducts(AGEs).Atthesametime,FGF21alsomarkedlyrenewedtheactivitiesofsuperoxidedismutase(SOD),catalase(CAT),glutathioneperoxidase(GPx)andtotalanti-oxidationcapability(T-AOC),anddecreasedtheenhancedtotalcholinesterase(TChE)activityinthebrainofd-gal-treatedmice.Theexpressionofaldosereductase(AR),sorbitoldehydrogenase(SDH)andmember-anchoredreceptorforAGEs(RAGE)declinedsignificantlyafterFGF21treatment.Furthermore,FGF21suppressedinflamm-agingbyinhibitingIκBαdegradationandNF-κBp65nucleartranslocation.Theexpressionlevelsofpro-inflammatorycytokines,suchasTNF-αandIL-6,decreasedsignificantly.Inconclusion,theseresultssuggestthatFGF21protectstheagingmicebrainfromd-gal-inducedinjurybyattenuatingoxidativestressdamageanddecreasingAGE17.Inhibitingreceptorforadvancedglycationendproduct(AGE)oxidativestressinvolvedintheprotectiveeffectmediatedbyglucagon-likepeptide-1receptoronAGEinducedneuronalapoptosisNeuroscienceLetters,Volume612,26January2016,Pages193-SongChen,LeiYin,ZhengXu,Feng-MaoAn,Ai-RanLiu,YingWang,BingYao,Xiang-DongOurpreviousstudyhasdemonstratedOurpreviousstudyhasdemonstratedthatglucagon-likepeptide-1(GLP-1)receptoragonistcouldprotectneuronsfromadvancedglycationendproducts(AGEs)toxicityinvitro.However,furtherstudiesarestillneededtoclarifythemolecularmechanismofthisGLP-1receptor-dependentaction.ThepresentstudymainlyfocusedontheeffectofGLP-1receptoragonistsagainstthereceptorforadvancedglycationendproducts(RAGE)signalpathwayandthemechanismunderlyingthiseffectofGLP-1.FirstlythedatabasedontheSH-GLP-1R+andSH-SY5YcellsconfirmedourpreviousfindingthatGLP-1receptorcouldmediatetheprotectiveeffectagainstAGEs.TheassaysoftheproteinactivityandofthemRNAlevelrevealedthatapoptosis-relatedproteinssuchascaspase-3,caspase-9,BaxandBcl-2wereinvolved.Additionally,wefoundthatbothGLP-1andexendin-4couldreduceAGEs-inducedreactiveoxygenspecies(ROS)accumulationbysuppressingtheactivityofnicotinamideadeninedinucleotidephosphate-oxidase.Interestingly,wealsofoundthatGLP-1receptoractivationcouldattenuatetheabnormalexpressionoftheRAGEinvitroandinvivo.Furthermore,basedontheanalysisoftheproteinexpressionandtranslocationleveloftranscriptionfactornuclearfactor-κB(NF-κB),andtheuseofGLP-1recepto