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1、MolNeurobiolDOI10.1007/s12035-013-8579-3AttenuationofEarlyBrainInjuryandLearningDeficitsFollowingExperimentalSubarachnoidHemorrhageSecondarytoCystatinC:PossibleInvolvementoftheAutophagyPathwayYizhiLiu&JiankeLi&ZhongWang&ZhengquanYu&GangChenReceived:30July2013/Accepted:24October2013#Spring
2、erScience+BusinessMediaNewYork2013AbstractCystatinC(CysC)isacysteineproteaseinhibitormayattenuateEBIandneurobehavioraldysfunctioninthisandpreviousstudieshavedemonstratedthatincreasingen-SAHmodel,possiblythroughactivatingautophagypathway.dogenousCysCexpressionhastherapeuticimplicationsonbr
3、ainischemia,Alzheimer’sdisease,andotherneurodegener-ativedisorders.OurpreviousreportshavedemonstratedthatKeywordsAutophagy.Subarachnoidhemorrhage.theautophagypathwaywasactivatedinthebrainafterexper-CystatinCimentalsubarachnoidhemorrhage(SAH),anditmayplayabeneficialroleinearlybraininjury(E
4、BI).Thisstudyinvesti-gatedtheeffectsofexogenousCysConEBI,cognitivedys-function,andtheautophagypathwayfollowingexperimentalIntroductionSAH.AllSAHanimalsweresubjectedtoinjectionsof0.3mlfresharterial,nonheparinizedbloodintotheprechiasmaticAneurysmalsubarachnoidhemorrhage(SAH)isadevastatingci
5、sternin20s.Asaresult,treatmentwithCysCwithlowdiseaseandcarriesamortalityraterangingfrom32%to67%andmedialconcentrationssignificantlyamelioratedthede-[1],whichaffectsapproximately137,200ChinesepeoplepergreeofEBIwhencomparedwithvehicle-treatedSAHrats.year(NationalScientificResearchProject201
6、1BA108B06,Microtubule-associatedproteinlightchain-3(LC3),abio-datanotpublished).Inthepastdecades,vasospasmhaslongmarkerofautophagosomes,andbeclin-1,aBcl-2-interactingbeenconsideredthemostdreadedcomplicationafterSAHandproteinrequiredforautophagy,weresignificantlyincreasedinalotofworkhasfoc
7、usedprimarilyonit.However,thehighthecortex48hafterSAHandwerefurtherup-regulatedaftermorbidityandmortalityassociatedwithSAHhavenotCysCtherapy.Byultrastructuralobservation,therewasachangeddespitemajoradvancesinsurgicaltechniques,radi-markedincreaseinautophagosomesanda
