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时间:2020-04-20
《银杏叶提取物后处理对大鼠局灶性脑缺血再灌注损伤保护作用的研究.pdf》由会员上传分享,免费在线阅读,更多相关内容在应用文档-天天文库。
1、卒中与神经疾病2014年8月第21卷第4期·219·银杏叶提取物后处理对大鼠局灶性脑缺血再灌注损伤保护作用的研究邓永超刘煜敏【摘要】目的探讨银杏叶提取物EGb761对大鼠局灶性脑缺血再灌注损伤的保护作用及其机制。方法制作大鼠右侧大脑中动脉闭塞再灌注模型。将3O只清洁级雄性SD大鼠随机分为3组,即假手术组(=10):给予5ml生理盐水腹腔注射;对照组(n=10):缺血90min,再灌注24h,5ml生理盐水腹腔注射;实验组(:10):缺血90min,再灌注24h,在再灌注即刻20mg/kg银杏叶提取物生理盐水稀释成5ml腹腔注射。再灌注24h后采用四
2、分法测定大鼠的神经功能障碍评分(NDS);实验结束后断头取脑采用TTC染色法测定脑梗死面积(以其同侧大脑半球体积的百分比表示);采用westernblot测定脑组织微管相关蛋白2(MAP2)的表达水平。结果与假手术组比较,对照组、实验组小鼠NDS评分均显著升高,分别为(2.49±0.85)分和(1.58±0.62)分,3组间比较差异均明显(P<0.05);对照组、实验组脑梗死面积均显著增大(P<0.05),实验组脑梗死面积较对照组显著减小(P<0.05);与假手术组比较,与假手术组比较,对照组、实验组缺血侧MAP2蛋白的表达水平均显著降低(P<0.
3、05),实验组缺血侧MAP2蛋白的表达水平较对照组显著升高(P4、tioningonthefocalcerebralischemiareperfusioninjuryinratsDengYongchao,LiuYumin.DepartmentofNeurology,ZhongnanHospitalofWuhanUniver—sity,Wuhan435200[Abstract]ObjectiveToexploreneuroprotectiveeffectsandpossiblemechanismsofextractofGinkgobilobapostconditioningonthefocalcerebralisc5、hemiareperfusioni~uryinrats.Methods30adultmaleSDratswererandomlydividedinto3groups(7z10):sham:normalsalineintraperitonealinjected;Controlgroup:cerebralischemia90min,reperfusion24h,normalsalineintraperitonealinjected;Experimentgroup:cerebralischemia90min,reperfusion24h,ratswere6、intraperitonealinjected20mg/kgofginkgobilobadilu—ted5mlinimmediatereperfusion.Themodelofrightmiddlecerebralarteryocclusion(MACO)andreperfu—sionwasmade.At24hourafterreperfusion,theneurologicdeficitscores(NDS)wereevaluatedusingafourpointscale.Attheendof24hreperfusion,theratwerea7、nesthetizedandsacrificedbydecapitation.Thebrainswererapidlyremovedformeasuringthecerebralsize(n5)andtheexpressionofMAP2(n5).Thecerebralinfartsizewasexpressedasapercentageoftheareaatipsilateralhemisphere.Results1NDS:com—paredwithshamgroup,NDSvaluesingroupcontrolgroupandexperime8、ntgroupincreasedsignificantly(P<0.05),comparedwithcontrolgrou
4、tioningonthefocalcerebralischemiareperfusioninjuryinratsDengYongchao,LiuYumin.DepartmentofNeurology,ZhongnanHospitalofWuhanUniver—sity,Wuhan435200[Abstract]ObjectiveToexploreneuroprotectiveeffectsandpossiblemechanismsofextractofGinkgobilobapostconditioningonthefocalcerebralisc
5、hemiareperfusioni~uryinrats.Methods30adultmaleSDratswererandomlydividedinto3groups(7z10):sham:normalsalineintraperitonealinjected;Controlgroup:cerebralischemia90min,reperfusion24h,normalsalineintraperitonealinjected;Experimentgroup:cerebralischemia90min,reperfusion24h,ratswere
6、intraperitonealinjected20mg/kgofginkgobilobadilu—ted5mlinimmediatereperfusion.Themodelofrightmiddlecerebralarteryocclusion(MACO)andreperfu—sionwasmade.At24hourafterreperfusion,theneurologicdeficitscores(NDS)wereevaluatedusingafourpointscale.Attheendof24hreperfusion,theratwerea
7、nesthetizedandsacrificedbydecapitation.Thebrainswererapidlyremovedformeasuringthecerebralsize(n5)andtheexpressionofMAP2(n5).Thecerebralinfartsizewasexpressedasapercentageoftheareaatipsilateralhemisphere.Results1NDS:com—paredwithshamgroup,NDSvaluesingroupcontrolgroupandexperime
8、ntgroupincreasedsignificantly(P<0.05),comparedwithcontrolgrou
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