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OALib Journal期刊
ISSN: 2333-9721
费用：99美元
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丁基苯酞对局部脑缺血大鼠行为和病理改变的保护作用
, PP. 896-903
Abstract:
观察了丁基苯酞对大鼠右侧大脑中动脉阻断(mcao)后行为和脑梗塞面积的影响。结果表明,mcao后15min丁基苯酞po或ip,均能降低局灶型脑缺血大鼠的脑梗塞面积和改善各种神经症状,疗效与mk801(0.5mg·kg-1,ip)相当,优于尼莫地平(1.0mg·kg-1.sc)。提示丁基苯酞可能是一个有开发前途的抗脑缺血药物。
| [1] | dl-3-n-butylphthalide(nbp)wasknowntohaveimprovingeffectonbrainenergymetabolismafterischemiainsult.thepurposeofthisstudyistodetermineifthedrughasprotectiveactionagainstischemicneuronaldamage,inthepresentstudy,theeffectofnbponcerebralinfarc-tionandneurologicaldeficitsaftermiddlecerebralarteryocclusion(mcao)inratswasinvestigated.focalcerebralischemiawaspreducedbypermanentocclusionoftheproximalportionoftherightmiddlecerebralartery(mca)accordingtothetechniqueoftamura.theinfarctareawasmeasuredby2,3,5-triphenyltetrazoliumchloride(ttc)stainingtechnique.theextentofneurologicaldeficitswasevaluatedbythemethodofbederson[2].thehistologicalchangesinneuronalchangeaftermcaoinratswerealsostudied.theresultsindicatethattheinfarctareaandthescoreofneurologjcaldeficitsaftermcaowerereducedsignificantlyfollowingintraperitonealpretreatmentorpre-andpot-treatmentwithnbp20mg·kg-1.thetreatmentwithnbp10or20mg·kg-1(ip),or20,40or80mg·kg-1(po)15minandeven2h(20mg·kg-1,ip)aftermcaoalsomarkedlyreducedtheinfarctareaandthescoreofneurologicaldeficits.however,noeffectwasfoundwhennbp(20mg·kg-1)wasinjectedintraperitoneally4haftermcao,mk-801(0.5mg·kg-1,ip),anon-competitiveantagonistofnmdareceptor,significantlyreducedthesizeofinfarctionandthescoreofneurologicaldeficitsinratssubjectedtomcao,thepotencyofnbpinreducingtheinfarctareaandneurologicaldeficitswasfoundtobequitesimilartothatofmk-801(0.5mg·kg-1,ip).noneuroprotectiveeffectofnimodipine(1.0mg·kg-1,sc)wasfound.generally,thepotencyofnbpinprotectingratsfromischemicneurologicaldamageisequaltothatofmk-80landismorepowerfulthanthatofnimedipine,sideeffectsofnbpinbehaviorwasnotfound.therefore,nbpseemstobeahopefuldrugforthetreatmentofstroke.
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