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1、硕士学位论文higherinmodelgroup(P<0.01).Piceid—treated,likeorevenbetterthanPTX.treated.soundlymaintainedtheultrastructureoftheinjuredcerebralinarelativelygoodappearance.PiceidsignificantlysuppressedLDproductionandMAOactivity,andatthesametime,PiceidobviouslypreventedreductionofSODac
2、tivity,reducedMDAproductionandinhibitedET-1contentintheinjuredcerebraltissueincomparisonwiththe1/Rmodelatthedoseof7.5,15and30mg/kg,withthemostremarkableeffectsappearingat24hafterI/R.Comparedwithshamgroupand3Piceidgroups,theinfarctsizesofthecerebralweremuchlargerinmodelgroup,
3、expressionofeNOSwasnotobserved,butinanothergroups,eNOSimmumoreactivityinneuronsofischemicterritorywasupregulated.Andalso,Piceidcouldpreventplateletsfrominhibitthereleasingreactions(P
4、oodpressuremeasurement.RecordthevaluesofCVR,MBPandCBFforeachlocationbeforeocclusion(baseline),and30minutesafterinductionofischemia(occlusion).OcclusionindogsresultedinsignificantlylessofdecreaseofCVRandMBPinthedogs.Andatthetime,PiceidobviouslypreventedreductionofCBF.Similarl
5、y,theexperimentsinvitrodemonstratedthatIL-1B·induced,TheexpressionofICAM·1wasmarkedlyincreased.Theexpressionof1CAM一1wasconfirmedinREMECbyELISA,whichshowedICAM一1expressiontobeincreased.PiceidcoulddirectlyandeffectivelyprotecttheRCMECfromthesedamagesthrou曲inhibitingtheexpressi
6、onofICAM一1.CONCLUSIONSPiceideffectivelyrepressedtissueedema,removedoxygenfreeradical;blockedlipidperoxidationandimprovedenergeticmetabolicsystemtoraisetheexpressionofeNOSSOastofurtheramelioratethelightmicroenvironment,whichwereinvolvedintheprotectiveinfluencesofPiceidonthece
7、rebralstructure,cellmorphology,andfunctionalrepairandevenneuronregenerationaftercerebraltrauma-TheeffectsofPiceidwerethesameasorgreaterthanthoseofPTX.AlltheresultsABs’rRACTsuggestedthatPiceidhaspotenttherapeuticeffectsinI/Rviaanoxygenfreeradical.Ca2+-NOpathway.KEYWORDSPiceid
8、;lschemia-repeffusioninjury;Secondaryedema;Ultrastructural;Lacticacid;Malon
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