乌司他丁对脑缺血再灌注大鼠脑组织细胞色素c、凋亡诱导因子表达与凋亡细胞数的影响

《乌司他丁对脑缺血再灌注大鼠脑组织细胞色素c、凋亡诱导因子表达与凋亡细胞数的影响》由会员上传分享，免费在线阅读，更多相关内容在行业资料-天天文库。

AbstactEffectsofUlinastatinonexpressionofcytochromeJ1-’-一1●p‘C．apootosis|nducingtactorandnumber0tapoptosisinbraintissueofratswithcelebral■l●n■●tscilemia-reperluslonInlUrVPostgraduate：LiuQing-jieSupervisor：Prof．BaiHong-yin91Prof．WangYu．zhou21DepartmentofNeurology,theSecondClinicalCollegeofZhengzhou2TheCentralHospitalofJiaozuoCoalGroupZhengzhou，Henan,China450014AbstractBackgroundand0bjectivesStrokeisoneofthethreefataldiseases，whichhasthe”threehigh”characteristicsofhighincidence，highmorbidityandhighmortality．Itcouldseriouslyaffectpeople’Squalityoflifeandbringheavyburdenstotlleirfamiliesandcountries．Strokeisdividedintoischemicstrokeandhemorrhagicstroke，Ischemicstrokeaccountsformorethan80％ofs仃oke，effectivetherapiesofischemicstrokerequirerecanalizationofoccludedcerebralbloodvessels，reperfusionofischemicbraintissueCancausecomplexprocessofreperfusioninjury,whichcanacceleratecelldeath．Apoptosisisconsideredoneoftheimportantmechanismesofcerebralischemiaandreperfusioninjury．Apoptosisisalsocalledprogrammedcelldeath(PCD)，therearethreemainapoptosispathways：mitochondriamediatedapoptosispathway,deathreceptormediatedapoptosispathwayandtheendoplasmicreticulumstress．Amongofthernthemitochondnalpathwayplaysanimportantrole．Themitochondria-mediatedapoptosispathwayincludescaspase-dependentandcaspase-independent．LotsofproteasesareIV Abstactreleasedfromthemitochondriatopromoteapoptosis．Ulinastatinisaproteaseinhibitor,whichcaninhibittrypsin，plasminandotherenzymes，inhibitthereleaseoflysosomalenzymesbystabilizingthelysosomalmembrane，inhibitetheproduceofmyocardialdepressionfactor,andwhichalsohasthefunctionsofscavengingoxygenfreeradicalsandinhibitingthereleaseofinflammatorymediators．Ulinastatinwasusedinthetreatmentofpancreatitisandlungdiseases．Inrecentyears，therewerereportsthatUlinastatinWasbeusedinthetreatmentofcerebrovasculardiseasedependentsonitsantioxidantandanti-inflammatorymechanism．UlinastatiniSstillunclearaboutitsspecificmechanismofapoptosis．Thefocalcerebralischemia-reperfusioninjurymodelofratswasestablished-withmiddlecerebralarteryocclusionbythreadligation．ThetreatmentgroupreceivedUTIbyintraperitonealinjection．ToinvestigatetheeffectsofUlinastatinonexpressionofcytoctunDmec'apoptosisinducingfactor(AIF)andthenumberofapoptosisinbraintissueofratswithcerebralischemia-reperfusioninjury．MaterialsandmethodsFiRy-fourhealthymaleSDratswhichweighted250—3009wererandomlydividedintoshamoperationgroup，ischemia-reperfusiongroup(controlgroup)，cerebralischemia-reperfusionandulinastatintreatmentgroup(treatmentgroup)．Everygrouphas18rats．Thefocalcerebralischemia-reperfusioninjurymodelofratsWasestablishedwithmiddlecerebralarteryocclusionbythreadligationreferencedfromZea-Longa'swithimprovement，excepttheshamegroup．ThecontrolgroupandthetreatedgroupWeregeneratedbyocclusionoftheleftMCAfor2hfollowedby24hofreperfusion，thetreatmentgroupreceivedUTI20000lU／kgbyintraperitonealinjectionassoonasthereperfusion，theothertwogroupsWeregiventhesamedoseofsaline．Theexpressionofcytcinbraintissueofratswasdetectedwithimmunohistologystaining，theexpressionofAIFinbraintissueofratsWasexaminedbyRT-PCR，thenumberofapoptosisinbraintissueofratswasanalyzedwithTuneltechnique．Allthedatawereexpressedas工4-s，SPSS17．0softwarewasusedtoanalysethisdatas．Thesinglefactoranalysisofvariancewasusedtocarryouttheinnergroupcomparisons．Thesignificantdifferencewasjudgedbya=0．05．ResultsV Abstact1．E肫ctsofUlinastatinonexpressionofcytochromeCinbraintissueofratswithcelebralischemia·reperfusioninjuryThepositivecellcountsofc”ochromeCinShamgroup，controlgroupandtreatmentgroupare3．20-a：O．75，98．40士7．28and74．804-3．37respectively．TheexpressionofcytCinbraintissueofratsinthecontrolgroupandtreatmentgroupweresignificantlyhigherthanwhichintheshamoperationgroup(p