大豆异黄酮对氧化损伤血管内皮细胞的抗氧化作用

ISSNI67I一5926CN2II470R咖础C帅删眦C帅刘英华，等大豆异黄酮对氧化损伤血管内皮细胞的抗氧化作用CULTUREANDEVALUATIONOFENDOTHELIALCELLSANERANABIOSISHEFROZENENDOTHELIALCELLSWASINOCULATEDINTLLECELLCULTURALBOARDWITLLEAGIESCUITUREMEDIUMMODIEDBYDULBECCOCONTAINING100GLFETALBOVINESEMM1ANDTHENCULTUREDINTHEINCUBATOROF37，50MLLC02，950MLLAIRSATURATEDHUMIDTY1HECELLSGREWTOFLUSEINTOPYKNOMONOIAYERANDTHENTHECULTURENUIDWASSLOPPEDTOBEREMOVEDTHEYWEREDJGESTEDWITHTHEEQUIVALENCEMIXTURESOF25GLTRYPSINAND2GLEDATHAMILANDTHENSUBCUTURDWITH12RHECEIISGROWINGTOFLUSEINTOMONOLAYERWEREUSEDINTHEEXPERIMENTSOLUTIONOFVITAMINEANDSOVBEANISONAVONETHEMIXTURESOFABSOIUTEAICOHOIANDDIMETHVISULF0XIDEWERUSEDTODISSOLVEDOSAGEGR0UPINGTHEEXPERIMENTWASDIVIDEDINTO6GMUPSBLANKCONTMLGMUP，OXIDATIVEDAMAGECONTMLGMUPMALONDIALDEHYDECONTENTWAS1MOIL】，OXIDATIVEDAMAGEVITAMINECONTMIGMUPVITAMINEWAS50MOLLANDOXIDATIVEDAMAGESOYBEANISONAVONE10，50，100MOLLCONTR0LGMUPRESEAR_CHMETHODTHECEIISOFGMWINGTOFUSEINTOTHEMONOIAYERWEREG0TTOSLOPPETOREMOVETHECULTURENUIDANDWASHEDF0R2OR3TIMESWITHBUFLFERPHOSPHATETHECELLCULTUMLNUIDWASRENEWEDANDVITAMINEANDSOVBEANISONAVONEWEREIOINEDTOINCUBATEFL0R24HOURSINADVANCEACCORDINGTOTHEDEMANDOFDOSAGEGMUPINGINTHEEXPERIMENTITWASCONTINUALTOBECUTUREDF0R24HOURSAGAINWITHTHEOXIDIZEDIOWDENSITYIIPOPROTEINAFTERDEGEMLINGIHECUTUREWASENDEDANDTHECELLSWERECOLLECTEDTHEANTIOXIDATIVEINDEXWASDETEMLINEDDETEMLINATIONOFTHEANTIOXIDATIVEINDEXANERTHEENDOFCEIICUITURE，THESUPEMATANTWASCOUECTEDWITHCENTRIFUGATIONWHENTHESPALLATIONOFCULTURENUIDANDCELLSTHEMETHODOFDISTILLEDWATERFOZEANDDEIIQUESCEDREPEATEDIYWEILEDONEEACHANTIOXIDATIVEINDEXOFCEUCULTURENUIDEXTRACEUULARANDSUPEMATANTINTILACEUULARWASDETEMLINEDSEPARATELVTHERESULTWASEXPRESSEDWITH12BORESOFCEIIUIARDATAOFEACHGROUPDETEMLINATIONOFMALONDIALDEHVDECONTENT，ACTIVITVOFSUPEROXIDEDISMUTASEANDACTIVITYOFGLUTATHIONEPEROXIDASETHEDETEMLINATIONWASPMGRESSEDACCORDINGTOTHEINSTMCTIONOFTESTKITTHENUMERICALVALUEOFEACHINDEXINSIDEANDOUTSIDETHECELLSWASCALCULATEDWITHTHEINCOMEABSORBANCEANDTHEDROTEINICCONCENTILATIONOFCE1IUIARENDOCHVIEMA。WHICHWASDETEMLINEDWITHTHEBIOTINSTREPTA。VIDINMETHODDETEMLINATIONOFTHERELEASECONDITIONOFLACTATEDEHVDRO盛ENASETHEDETEMLINATIONWASPROGRESSEDACCORDINGTOTHEINSTMCTIONOFTESTKITTHERELEASEPERCENTAGEOFLACTATEDEHYDROGENASEWASCALCULATEDWITHTHEINCOMEABSORHANCERELEASEPERCENTAEOFLACTATEDEHVDRO只ENASEABSORBANCEOFCEIIUIARCUITURENUIDFABSORBANCEOFCEUULARCULTURENUIDABSORHANCEOFCEUULARSUPEMATANT1100DETEMLINATIONOFNITMGENMONOXIDUMCOENTTHEDETEMLINATIONWASPMGRESSEDACCORDINGTOTHEINSTMCTIONOFTESTKITTHECONCENTMTION0FNITMGENMONOXIDUMINSIDEANDOUTSIDETHECELLSWAS171CALCULATEDWITHTHEINCOMEABSORHANCECOMBINEDWITLLTLLEPR0TEINICCONCENTRATIONINENDOCHYLEMASTATISTICALANALYSISSPSS100SOFHAREPAEKAGEW_ASUSEDTOPE卜F0MITHEDATAPMCESSINGBYTLLEFIRSTAUTLLOR0NEWAYANALYSISOFVANCEWASUSEDTOMAKECOMPSONRESULTSHINUENOEOFSOYBEANIS0AAVONEONMALONDIALDIMYDIC0NTENTACTIESOFSUPERODE蜘UTAANDGIU纽THIO眦PER0嫡凼ISEINTHEENDOTHELIALCELIS0FO嫡DAVEDAMAGEABLE1TABLE1SHOWEDTHATTLLEDI珏LERENCESOFEACHMUPALLWEREOFSIGNIFICANCEINTHE3INDEXESWHETHERTHEYWEREINCELLULAROREXTMCELLULAR001AMONGTLLEM，THEMAL0NDIALDEHYDECONTENTWASHIGHERSIGNIFICANTLYINOXIDATIVEDAMAGECONTRDLGMUPTHANINBLANKCONTROLGROUPP001，BUTTHEACTIVTYOFSUPEROXIDEDISMUTASEORGLUTATHIONEPEROXIDASEWASLOWERSIGNIFICANTLYINOXIDATIVEDAMAGECONTROLGMUPTHANINBLANKCONTROLGMUPP001VITAMINEANDSOYBEANISONAVONEWEREADDEDINADVANCETOMAKETHEMALONDIALDEHYDECONTENTRDUCEP001ANDTHEACTIVITYOFSUPER0XIDEDISMUTASEANDGLUTATLLIONEPEMXIDASEINCREASE001INNUENCE0FSOYBEANIS0FIAV0NE蚰THEREI朗SECONDI廿ONOFIACTATEDEHYDROGENASEANDTHEPR0D喇VEQU删TY0FIIITR0GENMON0XIDEINTHEEND0恤LIAICELIS0FO嫡DA廿VED啪AGERABLE2IIE2SHOWEDTHAT，INCOMPARIS0NOFTHEREIEASEPERCENTAGEOFIACTATEDEHYDROGENASEANDTHEPRODUCTIVEQUANTITYOFNITROGENMONOXIDEBETWEENGMUPS，THEDIRENCESWEREOFSIFICANCE001AM0NGTHEM，THEREIEASEPERCENTAGEOFIACTATEDEHYDMGENASEWASHIGHERSIGNIFICANTLYINOXIDATIVEDAMAGECONTROLGMUPTLLANINBLANKCONTROLGMU001，BUTTHEPRODUCTIVEQUANTITYOFNITRDGENMONOXIDEWASIOWERSIGNIFICANTIYINOXIDATIVEDAMAGECONTMIGMUPTHANINBLANKCONTRDLGMUPP001VITAMINEANDSOYBEANISONAVONEWEREADDEDINADVANCETOMAKETHERELEASEPERCENTAGEOFIACTATEDEHYDMGENASEREDUCESIGNIFICANTIY尸001ANDTHEPRODUCTIONOFNITMGENM0N0XIDEINCREASESIGNIFICANTLY001DLSCUSSIONTHERESEARCHINDICATESTLLATTLLEDAMAGEOFENDOTLLELIALCELLSANDDISFUNCTIONOFTHEMARETLLEBE舀NNINGSTOPPINGLINKINTHEF0MLATIONOFATHEROSCIEROTICIESIONANEXCESSOFIOWDENSITYIIPOPROTEINSINTHEBLOOD，ESPECIAUYOXIDIZEDLOWDENSITYLIPOPROTEIN，ISANIMPORTANTHAMLFULFACTORTLLATCAUSESTHEDAMAGEOFENDOTLLELIALCELLTHEEXPERIMENTAISTUDIESINRECENTYEARSPROVETILATTHEOXIDIZEDLOWDENSITYLIPOPIL0TEINHASCYTOTOXICITY，WHICHMAYINDUCETLLEDAMAGEOFENDOTHELIALCELLSTHISEXPERIMENTFINDS，INTHEENDOTHELJALCEIISOFOXIDIZEDIOWDENSITYIIPOPROTEINGMUP，THEMAIONDIAIDEHYDECONTENTISVERYHIGH，TLLEACTIVITYOFSUPEROXIDEDJSMUTASEANDGLUTATLLIONEPER0XIDASEAREVERYLOW，THERELEASEPELCENTAGEOFLACTATEDEHYDROGENASEISHIGHCOMPARATIVEIY，THECONCENTRATIONOFNINL0GENMONOXIDUMISLOWCOMP啪TIVELYANDTLLEDIFRERENCESHAVESIGNIFICANCEASCOMPAREDWITHTHEBLANKCONTR_0LGMUP001，WHICHTABLELC0MPS0N0FMAL0NDDEHYDEC0NTENT，ACTIVITY0FSUPEROXIDEDIS咖TASEANDGLUTATHI0NEPER0XIDASEINSIDEAND0USIDETHE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