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1、宁夏医科大学硕士研究生论文英文摘要Uncouplingprotein2playaroleinhyperglycemiaaggravatedcerebralischemia-reperfusioninjurymediatedbythemitochondriaABSTRACTObjectiveDiabeteshyperglycemiaaggravatedcerebralischemia-reperfusioninjury,andpromotedproductionofmitochondrialreactiveoxygenspecies(ROS)afterischemia.Uncouplingpr
2、otein2(UCP2)canstabilizedthemitochondrialmembranepotentialandreducedthegenerationofROS.Butatpresent,mechanismofactionandregulatorypathwayofUCP2inhyperglycemiaaggravatedcerebralischemiainjuryarenotclear.ThisstudyusingUCP2knockoutmicesimulatedcerebralischemiaandhyperglycemia,toexploreifUCP2knockoutca
3、naggravatedneuronalinjuryanditsmolecularpathways.MethodsMaleUCP2knockoutmice(KO-UCP2)andwild-typeC57BL/6jmicewererandomlydividedintowild-typemicewithnormoglycemicfocalcerebralI/Rgroup(CNgroup),KO-UCP2micewithnormoglycemicfocalcerebralI/Rgroup(KNgroup)andKO-UCP2micewithdiabetichyperglycemicI/Rgroup(
4、KHgroup).AtypeⅠdiabeticratmodelwasinducedbystreptozotocin(STZ)injectionandthefocalcerebralI/Rmodelwasinducedby1hourofmiddlecerebralarteryocclusion(MCAO)followedby6h,24h,72hofreperfusion.Histopa-thology,immunohistochemistry,immunofluorescence,TTCstaining,TUNEL,RT-PCRandwesternblotwereappliedtodetect
5、changesofthemorphologyandthenumberofneurons,apoptosisandtheexpressionofCytC,CleavedCaspase-9,Caspase-3fromeachgroup.Results(1)At24hofI/R,thebrainfunctionscoresofKNgroupwerehigherthanCNgroup(P<0.05),andKHgroupwereobviouslyhigherthanKNgroupIII万方数据宁夏医科大学硕士研究生论文英文摘要(P<0.05).(2)TTCstainingresultsshownno
6、significantinfarctioninshamgroup.At24hofI/R,infarctsizeofKNgroupwassignificantlylargerthantheCNgroup,andKHgroupwaslargerthantheKNgroup(P<0.05).(3)Brainedemaandpartialshrinkageofneuronswereobservedininfarctionareaat6hourI/Rafter1hofischemiaandworseddamage,structuralfailure,disorderarrangementat24hou
7、rofI/R.At72h,necroticnervecellsheddingandappearedInflammatorycellsandalargenumberofglialcellsininfarctionarea.ComparedwithCN,KNgroup,evenworsecerebraledemawasdetectedinKHgroup.Aroundtheinfarctionarea,penumb