简介：AIMTheformationofadvancedglycationendproducts(AGEs)onconnectivetissueandmatrixcomponentsleadstoincreasesincollagencrosslinkingthatcontributestoaorticandmyocardialstiffnessinnormalagingandwhichoccursatanacceleratedrateindiabetes.Inthisstudy,weexaminedtheeffectsofanovelAGEsbreaker,C36,oncardiovasculardysfunctionsinexperimentaldiabeticrats.METHODSandRESULTSMaleWiatarratsweremadediabeticbyi.p.injectionof70mg/kgstreptozotocin.After12weeksofdiabetes,theanimalswererandomlydividedinto4groups(n=8-11),

简介：AIMToinvestigatetheexpressionchangeofα-synucleininthebrainofdifferentageAD-likean-imalmodelandtoexplorethepathologymechanismofα-synucleininneuraldegenerationandprotectiveeffectof2kindsofChinesecomponents.METHODSAgenerallyacceptedanimalmodelofAlzheimer'sdisease-APPV717Itransgenic(Tg)mousewasobservedfrom4to16monthold.TheTgmicewererandomlydividedintomodelgroup(4month,10monthand16monthold),Shen-wucapsulewiththedoseof0.4gand1.2g/kg/d,2,3,5,4’-tetrahydroxystilbene-2-O-β-D-glucoside(TSG),oneofeffectivecomponentsinPolygonummuhiflorum,atdoseof0.05,0.1and0.2g/kg/d.