转bcl-2基因大鼠全脑缺血再灌注后c-Myc蛋白的表达  

Expression of c-Myc protein in hippocampus of bcl-2 transgenic rats after global cerebral ischemia/reperfusion

作　　者：李伟[1] 薛荣亮[1] 

机构地区：[1]西安交通大学医学院第二附属医院麻醉科,西安710004

出　　处：《山西医科大学学报》2011年第10期793-796,855,共5页Journal of Shanxi Medical University

基　　金：国家自然科学基金资助项目(30070731)

摘　　要：目的研究转bcl-2基因大鼠全脑缺血灌注后c-Myc蛋白在海马回的表达。方法健康雄性SD大鼠随机分为三组:缺血再灌注组(IR,n=30),采用4-血管法建立全脑缺血再灌注模型,全脑缺血6 min后再灌注;假手术组(SO,n=30),只暴露血管而不夹闭;转bcl-2基因模型加缺血再灌注组(bcl-2,n=30)。各组动物于6,12,24,48,72,96 h以4%多聚甲醛灌注处死,将脑组织切片进行TUNEL染色和HE染色,光镜下观察海马回神经元形态结构改变、c-Myc在CA1和CA3区不同表达及阳性神经细胞数,进行统计学分析。结果①全脑缺血再灌注后6 h,c-Myc在IR组CA1及CA3区均有表达,48 h表达强度最高,72 h后强度下降,CA3区弱于CA1区,主要位于胞质,bcl-2组c-Myc表达强度均弱于IR组。②HE染色显示,全脑缺血再灌注后72 h,IR组CA1区组织水肿明显,神经元数目减少,排列混乱,核膜不清,核仁消失,CA3区神经元改变较轻,bcl-2组损伤较微。③TUNEL染色结果显示,IR组全脑缺血再灌注后24-48 h海马CA1区凋亡阳性细胞数最多,至再灌注后72h,海马CA1区凋亡阳性细胞数减少,bcl-2组凋亡阳性细胞均较少。结论 c-Myc蛋白在全脑缺血再灌注后海马回CA1区及CA3区都有表达,只是强弱及细胞分布不同,bcl-2可通过抑制c-Myc的表达抑制凋亡。Objective To investigate the expression of c-Myc protein in hippocampus of bcl-2 transgenic rats after global cerebral ischemia/reperfusion. Methods Ninety healthy male SD rats were randomly assigned into 3 groups.In ischemia/reperfusion group（IR group,n=30）,global cerebral ischemia/reperfusion model was established by 4-VO method.Global cerebral ischemia was performed for 6 min,and then carotid artery blood flow was restored.In sham operation group（SO group,n=30）,blood vessels were just exposed but not occluded.In bcl-2 group（n=30）,the bcl-2 transgenic rat model was established,and then global ischemia/reperfusion model was induced using the same way as IR group.All animals were executed at 6,12,24,48,72 and 96 h by 4% poly-formaldehyde perfusion.TUNEL and HE staining of brain tissue section were used to observe the morphological change of hippocampus,and detect the expression of c-Myc protein in CA1 and CA3 region of hippocampus,and the number of c-Myc positive nerve cells.All the data were analyzed by SPSS 10.0. Results ①The expression of c-Myc protein was detected in CA1 region in IR group at 6 h after global cerebral ischemia/reperfusion,and peaked at 48 h,and c-Myc protein was mainly localized in cell plasma.The expression of c-Myc protein in CA3 region was weaker than that in CA1 region,and also localized in cell plasma.The expression of c-Myc protein in bcl-2 group was weaker than that in IR group at every time point.②HE staining showed that the number of neuron in CA1 region in IR group decreased at 72 h after global cerebral ischemia/reperfusion,companied with neuron disarrangement,nucleus membrane indistinction and nucleolus disappearance.The changes of neuron in CA3 region were lighter than that in CA1 region.However,the neuron damage in bcl-2 group was not obvious.③TUNEL staining showed that the positive number of apoptosis cell reached the peak at 24-48 h after global cerebral ischemia/reperfusion in CA1 region of hippocampus.The positive number of apoptosis cell in bcl-2 group was

关 键 词：缺血再灌注 C-MYC 海马 大鼠 凋亡 BCL-2 转基因 

分 类 号：R362[医药卫生—病理学]