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。

1、AbstactEffectsofUlinastatinonexpressionofcytochromeJ1-’-一1●p‘C．apootosis

2、nducingtactorandnumber0tapoptosisinbraintissueofratswithcelebral■l●n■●tscilemia-reperluslonInlUrVPostgraduate：LiuQing-jieSupervisor：Prof．BaiHong-yin91Prof．WangYu．zhou21DepartmentofNeu

3、rology,theSecondClinicalCollegeofZhengzhou2TheCentralHospitalofJiaozuoCoalGroupZhengzhou，Henan,China450014AbstractBackgroundand0bjectivesStrokeisoneofthethreefataldiseases，whichhasthe”threehigh”characteristicsofhighincidence，highmorbidityandhighmortality．I

4、tcouldseriouslyaffectpeople’Squalityoflifeandbringheavyburdenstotlleirfamiliesandcountries．Strokeisdividedintoischemicstrokeandhemorrhagicstroke，Ischemicstrokeaccountsformorethan80％ofs仃oke，effectivetherapiesofischemicstrokerequirerecanalizationofoccludedce

5、rebralbloodvessels，reperfusionofischemicbraintissueCancausecomplexprocessofreperfusioninjury,whichcanacceleratecelldeath．Apoptosisisconsideredoneoftheimportantmechanismesofcerebralischemiaandreperfusioninjury．Apoptosisisalsocalledprogrammedcelldeath(PCD)，t

6、herearethreemainapoptosispathways：mitochondriamediatedapoptosispathway,deathreceptormediatedapoptosispathwayandtheendoplasmicreticulumstress．Amongofthernthemitochondnalpathwayplaysanimportantrole．Themitochondria-mediatedapoptosispathwayincludescaspase-depe

7、ndentandcaspase-independent．LotsofproteasesareIVAbstactreleasedfromthemitochondriatopromoteapoptosis．Ulinastatinisaproteaseinhibitor,whichcaninhibittrypsin，plasminandotherenzymes，inhibitthereleaseoflysosomalenzymesbystabilizingthelysosomalmembrane，inhibite

8、theproduceofmyocardialdepressionfactor,andwhichalsohasthefunctionsofscavengingoxygenfreeradicalsandinhibitingthereleaseofinflammatorymediators．Ulinastatinwasusedinthetreatmentofpancreatitisandlungdiseases．Inrecentyears，therewerereportsthatUlinastatinWasbeu

9、sedinthetreatmentofcerebrovasculardiseasedependentsonitsantioxidantandanti-inflammatorymechanism．UlinastatiniSstillunclearaboutitsspecificmechanismofapoptosis．Thefocalcerebralischemia-reperfusioninjurymodelof