bFGF对大鼠脑缺血再灌注后神经元凋亡及fractalkine表达的影响  

Effects of bFGF on neuronal apoptosis and fractalkine expression in cerebral ischemia/reperfusion rats

作　　者：韩江全[1] 于奎营[1] 胡泳涛[1] 林冬融[1] 黄名璐[1] 

机构地区：[1]遵义医学院第五附属(珠海)医院神经内科,广东珠海519100

出　　处：《中国病理生理杂志》2011年第6期1222-1225,共4页Chinese Journal of Pathophysiology

基　　金：遵义医学院硕士启动基金资助项目(No.200826);珠海市重点学科项目(No.珠卫200880)

摘　　要：目的:观察碱性成纤维细胞生长因子(bFGF)对大鼠脑缺血再灌注缺血半暗带侧皮质区fractalkine表达的影响,进一步探讨bFGF的神经保护机制。方法:应用栓线法建立大鼠脑缺血再灌注模型,36只实验大鼠随机分为3组:假手术组、缺血再灌注组和bFGF组,缺血1 h再灌注24 h后行神经功能评分,TTC染色测梗死面积,TUNEL法检测细胞凋亡数目,免疫组化检测fractalkine表达,并进行图像分析。结果:缺血再灌注组及bFGF组的神经功能评分分别为3.18±0.65和2.23±0.59,两组比较P<0.05;假手术组、缺血再灌注组及bFGF组凋亡细胞数目分别为0.91±0.65、17.28±1.01及13.22±1.35,bFGF组的凋亡细胞数目较缺血再灌注组明显减少(P<0.05);假手术组、缺血再灌注组及bFGF组fractalkine表达量分别为101.26±1.13、113.17±1.35及107.25±3.25,与假手术组相比,缺血再灌注组fractalkine表达减少,bFGF组fractalkine表达量显著高于缺血再灌注组(P<0.05)。结论:bFGF的神经保护作用可能与其上调fractalkine表达水平有关。AIM：To study the effects of basic fibroblast growth factor（bFGF） on neuronal apoptosis and fractalkine expression in ischemic penumbra after cerebral ischemia/reperfusion in rats.METHODS： Thirty-six rats were randomly divided into 3 groups： sham operation group,ischemia/reperfusion group and bFGF group.The model of middle cerebral artery occlusion was established by the method of intraluminal filament blockage.The middle cerebral arteries were blocked for 1 h and then reperfused for 24 h.Neurological performances of all rats were scored with Bederson＇s standard.The brain tissues of the rats were stained and the average infarct volume was calculated.TUNEL method was used to determine the number of apoptotic neurons,and the expression of fractalkine was detected by the method of immunohistochemistry.RESULTS： The score of neurological performances in bFGF group was 2.23±0.59,lower than that in ischemia/reperfusion group（3.18±0.65）.The number of apoptotic neurons in bFGF group（13.22±1.35） was lower than that in ischemia/reperfusion group（17.28±1.01,P0.05）,which was the lowest in sham operation group（0.91±0.65）.Compared with sham operation group,the expression of fractalkine in ischemia/reperfusion group was decreased.The expression of fractalkine in bFGF group was mainly higher than that in ischemia/reperfusion group（P0.05）.CONCLUSION： Up-regulation of fractalkine may be one of the molecular mechanisms of bFGF to protect neurons against ischemia/reperfusion injury.

关 键 词：碱性成纤维细胞生长因子 缺血再灌注 细胞凋亡 

分 类 号：R363.271[医药卫生—病理学]