缺血后处理对大鼠脑缺血/再灌注后海马CA_1区神经元凋亡及β淀粉样蛋白1-40表达的影响  

Effect of ischemic postconditioning on neuron apoptosis and expression of β-Amyloid protein1-40 in hippocampus CA_1 region following cerebral ischemia/reperfusion in rats

作　　者：张迎[1] 王晔[2] 刘佳丽[2] 高丹丹[2] 席自中[2] 

机构地区：[1]辽宁医学院研究生学院,辽宁锦州121001 [2]沈阳军区总医院神经内科

出　　处：《中风与神经疾病杂志》2010年第2期131-134,共4页Journal of Apoplexy and Nervous Diseases

基　　金：沈阳军区总医院医药卫生科研基金资助项目(08Y-E05)

摘　　要：目的探讨缺血后处理(ischemic postconditioning,IP)对脑缺血/再灌注(ischemia/reperfusion,I/R)后大鼠海马CA1区神经元凋亡及β淀粉样蛋白1-40(β-Amyloid Prote in 1-40,Aβ1-40)表达的影响。方法40只雄性SD大鼠随机分为假手术(SH)组、I/R组、IP组。用线栓法建立大鼠大脑中动脉缺血模型,脑缺血60m in后进行不同时间点的缺血后处理,恢复再灌注24h后行神经行为学评分(NDS),检测神经元凋亡及Aβ1-40的表达。结果与I/R组比较,IP组显著改善NDS(P<0.01),显著减少海马CA1区神经元凋亡(P<0.01)及Aβ1-40表达水平(P<0.01)。Aβ1-40的表达与细胞凋亡呈正相关(r=0.845,P<0.01)。结论缺血后处理可通过抗细胞凋亡机制减轻脑缺血/再灌注损伤。缺血/再灌注后Aβ1-40表达上调,缺血后处理可减少缺血/再灌注后Aβ1-40表达。Aβ1-40可能参与缺血后处理抗细胞凋亡的脑保护机制。Objective To explore the effect of ischemic postconditioning on neuron apoptosis and expression of β-Amyloid protein 1-40（Aβ1-40）in hippocampus CA1 region following cerebral ischemia/reperfusion（I/R） in rats.Methods Forty male Sprague-Dawley rats were randomly divided into sham-operation（SH） group,I/R group and ischemic postconditioning（IP） group.Using thread embolism method to develop the model of focal cerebral ischemic reperfusion injury in rats.Rats were treated with postconditioning after 60 minutes of occlusion.Neurologic scores,the number of neuron apoptosis in hippocampus CA1 region and expressions of Aβ1-40 were assessed at 24 hours.Results Compared with I/R group,the neurologic scores in IP group decreased significantly（P〈0.01）,the number of apoptosis in hippocampus CA1 region in IP group decreased significantly（P〈0.01）,and the expressions of Aβ1-40 in the ischemic hippocampus CA1 region were upregulated significantly（P〈0.01）.There were significant positive correlations between the neuron apoptosis and expression level of Aβ1-40.Conclusions Those findings indicate that postconditioning inhibits focal cerebral ischemia/reperfusion injury.The expressions of Aβ1-40 do increased after ischemia/reperfusion.Ischemic postconditioning could downregulate the level of Aβ1-40.Its reveals that neuroprotective mechanism of postconditioning may be related with Aβ1-40.

关 键 词：缺血后处理 脑缺血/再灌注 凋亡 Β淀粉样蛋白1-40 

分 类 号：R743.3[医药卫生—神经病学与精神病学]