转bcl-2基因大鼠全脑缺血再灌注后海马CA1区P-P38的表达  

Expression of P-P38 in hippocampus CA1 region of bcl-2 transgenic rats after global cerebral ischemia reperfusion

作　　者：雷晓鸣[1] 张珍妮[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》2012年第9期645-648,721,共5页Journal of Shanxi Medical University

基　　金：国家自然科学基金资助项目(30070731);陕西省科学技术研究发展计划基金资助项目[2010k15-03(1)]

摘　　要：目的观察转bcl-2基因大鼠全脑缺血组再灌注后P-P38蛋白在海马回CA1区的表达。方法 90只健康雄性SD大鼠,随机分为三组:假手术组(SO组,n=30),暴露血管而不夹闭;缺血再灌注组(IR组,n=30),采用4-VO法建立全脑缺血再灌注模型,5 min缺血后给予再灌注;转bcl-2基因组(bcl-2组,n=30):大鼠经转基因处理后再缺血再灌注。各组动物于再灌注后2,6,12,24,48,72 h处死,将脑组织切片进行HE染色,免疫组化染色及TUNEL染色,观察海马回神经元形态改变,凋亡细胞数量及P-P38在CA1区表达。结果 HE染色显示:IR组全脑缺血再灌注后48 h CA1区神经元数目减少,排列紊乱,核膜界限不清,结构模糊;bcl-2组变化不明显。免疫组化染色显示:P-P38在SO组基本呈阴性着色;IR组CA1区2 h出现,48 h达高峰,72 h略有下降;bcl-2组P-P38表达趋势同IR组,但各时间点表达强度弱于IR组。TUNEL染色显示:SO组可见到少量凋亡细胞;IR组全脑缺血再灌注后48 h凋亡细胞数达高峰;bcl-2组再灌注后12-72 h凋亡细胞数量较IR组均明显减少。结论全脑缺血再灌注后海马CA1区P-P38表达增加,bcl-2可通过抑制P-P38表达抑制脑缺血再灌注后的细胞凋亡。Objective To investigate the expression of P-P38 in hippocampus CA1 region of bcl-2 transgenic rats after global cerebral ischemia reperfusion. Methods Ninety healthy male SD rats were randomly divided into sham operation group （SO group, n = 30 ） , is- chemia reperfusion group（ IR group, n = 30）and bcl-2 transgenic group （bcl-2 group, n = 30 ）. Blood vessels of rats in SO group were just exposed but not occluded ;the rats were induced to establish the global cerebral isehemia/reperfusion model by 4-VO method; the rats in bcl-2 group were performed as the same as IR group after establishment of the bcl-2 transgenic model. The rats were executed at 2, 6,12,24,48,72 h after reperfusion,respeetively. The neuronal morphology,cell apoptosis and the expression of P-P38 in hippocampus CA1 gyrus were examined by HE staining,TUNEL staining and immunohistochemical staining method. Results HE staining showed that the neuron in CA1 region in IR group decreased at 48 h after global cerebral ischemia reperfusion, companying with neuron disarrangement, nucleus membrane indistinction and nucleolus disappearance, however, no obvious changes were found in bcl-2 group. Immu- nohistochemical staining showed P-P38was negative in SO group, and expressed weakly in CA1 in IR group at 2 h after global cerebral isehemia reperfusion,then peaked at 48 h. Expression of P-P38 at each time point in bel-2 group was significantly weaker than that in IR group（P 〈0.05） ,although the expression trend in bcl-2 group was similar to that in IR group. TUNEL staining showed that only few apoptosis cells were found in SO group, while the positive apoptosis cells reached the peak at 48 h after global cerebral ischemia reperfusion in CA1 region of hippocampus in IR group. The positive number of apoptosis cell at 12 h,24 h,48 h,72 h after global cerebral ischemia reperfusion in bcl-2 group was much less than that in IR group （P 〈 0.05 ）. Conclusion P-P38 expression increases in hippocampus CA1 region after glohal ischemia reperfusion

关 键 词：全脑缺血再灌注 BCL-2 转基因 P-P38 

分 类 号：R363[医药卫生—病理学]