卒中与神经疾病
卒中與神經疾病
졸중여신경질병
2015年
4期
211-214
,共4页
刘鹏%王瑾%苗常青%刘玥%唐鹏%侯辰%张欣%种莉%李晓青%李锐
劉鵬%王瑾%苗常青%劉玥%唐鵬%侯辰%張訢%種莉%李曉青%李銳
류붕%왕근%묘상청%류모%당붕%후신%장흔%충리%리효청%리예
脑缺血%神经生长因子%脑源性神经营养因子
腦缺血%神經生長因子%腦源性神經營養因子
뇌결혈%신경생장인자%뇌원성신경영양인자
Cerebral ischemia injury%Nerve growth factor%Brain-derived neurotrophic factor
目的：观察大鼠局灶性脑缺血后大鼠神经行为、梗死体积、组织形态及缺血半暗带神经生长因子(NGF)、脑源性神经营养因子(BDNF)的表达水平变化。方法将健康雄性 SD 大鼠24只随机分为2组,Ⅰ组(假手术组)；Ⅱ组(脑缺血组)。用线栓法建立动物模型,不给予再灌注,各组在术后48h 断头取脑,处死前行神经功能评分,用氯化三苯基四氮唑(TTC)染色计算脑梗死体积,用 HE 染色观察组织学形态,用免疫组织化学染色观察 NGF、BDNF 的表达水平。结果Ⅰ组在神经功能评分、梗死体积、组织形态及大脑皮层相应部位 NGF、BDNF 阳性细胞数均正常。与Ⅰ组比较,Ⅱ组的神经功能评分和梗死体积均严重受损；光镜下Ⅱ组缺血性病理改变较重,与Ⅰ组比较,Ⅱ组缺血半暗带 NGF、BDNF 阳性神经元数增加(P <0.05)。结论脑缺血本身可上调缺血半暗带 NGF、BDNF 的表达水平。
目的：觀察大鼠跼竈性腦缺血後大鼠神經行為、梗死體積、組織形態及缺血半暗帶神經生長因子(NGF)、腦源性神經營養因子(BDNF)的錶達水平變化。方法將健康雄性 SD 大鼠24隻隨機分為2組,Ⅰ組(假手術組)；Ⅱ組(腦缺血組)。用線栓法建立動物模型,不給予再灌註,各組在術後48h 斷頭取腦,處死前行神經功能評分,用氯化三苯基四氮唑(TTC)染色計算腦梗死體積,用 HE 染色觀察組織學形態,用免疫組織化學染色觀察 NGF、BDNF 的錶達水平。結果Ⅰ組在神經功能評分、梗死體積、組織形態及大腦皮層相應部位 NGF、BDNF 暘性細胞數均正常。與Ⅰ組比較,Ⅱ組的神經功能評分和梗死體積均嚴重受損；光鏡下Ⅱ組缺血性病理改變較重,與Ⅰ組比較,Ⅱ組缺血半暗帶 NGF、BDNF 暘性神經元數增加(P <0.05)。結論腦缺血本身可上調缺血半暗帶 NGF、BDNF 的錶達水平。
목적：관찰대서국조성뇌결혈후대서신경행위、경사체적、조직형태급결혈반암대신경생장인자(NGF)、뇌원성신경영양인자(BDNF)적표체수평변화。방법장건강웅성 SD 대서24지수궤분위2조,Ⅰ조(가수술조)；Ⅱ조(뇌결혈조)。용선전법건립동물모형,불급여재관주,각조재술후48h 단두취뇌,처사전행신경공능평분,용록화삼분기사담서(TTC)염색계산뇌경사체적,용 HE 염색관찰조직학형태,용면역조직화학염색관찰 NGF、BDNF 적표체수평。결과Ⅰ조재신경공능평분、경사체적、조직형태급대뇌피층상응부위 NGF、BDNF 양성세포수균정상。여Ⅰ조비교,Ⅱ조적신경공능평분화경사체적균엄중수손；광경하Ⅱ조결혈성병리개변교중,여Ⅰ조비교,Ⅱ조결혈반암대 NGF、BDNF 양성신경원수증가(P <0.05)。결론뇌결혈본신가상조결혈반암대 NGF、BDNF 적표체수평。
Objective To observe the expression of neurotropic factors on a rat model of focal middle cerebral artery occlusion (MCAO).Methods Twenty-four male Sprague-Dawley rats were randomly divided into two groups,groupⅠ(Sham operated rats)and groupⅡ(MCAO ischemia).The neuroethology assessment was evaluated at 48h before the rats were executed and given reperfusion.The volume of cerebral infarction and the pathologic changes were observed by TTC staining and HE staining.The expression of NGF and BD-NF was tested by immunohistochemistry.Results Under optical microscope,group Ⅱhad more degree of cer-ebral ischemic injury in pathomorphology.The numbers of NGF and BDNF immunopositive neurons in ische-mic penumbra of groupⅡ were higher than those in cerebral cortex of groupⅠ (P <0.05).Conclusions Brain ischemia injury can increase the expression NGF and BDNF in the brain ischemic penumbra,bur its mechanism is not clear.
