白藜芦醇苷对大鼠急性脑缺血再灌注损伤的保护作用与机制-研究

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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