p63与大鼠全脑缺血后神经元凋亡的关系及肢体缺血后处理对p63表达的影响  

Relationship between p63 expression and neuronal apoptosis after cerebral ischemia and influence of limb ischemic postconditioning in rats

作　　者：廖常莉[1] 周述芝[1] 张英[1] 赵小蓉[1] 欧册华[1] 

机构地区：[1]泸州医学院附属医院麻醉科,泸州646000

出　　处：《临床与实验病理学杂志》2012年第12期1351-1355,共5页Chinese Journal of Clinical and Experimental Pathology

基　　金：四川省卫生厅科研课题(100289);泸州市科技计划项目[2010S14(3/14)]

摘　　要：目的探讨p63与大鼠全脑缺血后神经元凋亡的关系及肢体缺血后处理对p63表达的影响。方法将120只SD大鼠随机分3组(每组40只):假手术(Sham)组、全脑缺血/再灌注(global cerebral ischemia/reperfusion,I/R)组和肢体缺血后处理(limb ischemia postconditioning,LIPC)组。各组分别在手术后6、12、24、48和72 h处死8只大鼠,行神经行为学评分,检测p63基因表达、神经元密度及凋亡情况。结果 I/R组p63阳性率在术后12、24、48和72 h较Sham组同时相高,组内48 h最高(P<0.01);LIPC组与I/R组同时相相比,p63表达降低(P<0.05)。I/R组细胞凋亡指数(apoptosis index,AI)较Sham组增加(P<0.05),其中术后48 h最高(P<0.05);LIPC组与I/R组同时相比较,AI减少,但高于Sham组(P<0.05),组内比较差异无显著性(P>0.05)。结论 p63基因表达在全脑缺血/再灌注后呈先增加后减少的趋势,与神经元凋亡趋势基本一致,提示p63可能参与了神经元的凋亡;肢体缺血后处理具有脑保护作用,其机制可能与下调p63基因表达进而抑制神经元凋亡有关。Purpose To study the relationship between p63 and neuronal apoptosis after cerebral isehemia and intervention of lim- bisehemie postconditioning in rats. Methods 120 male SD rats were randomly divided into three groups, 40 in each group： Sham group, global cerebral ischemia/reperfusion （I/R） group and limb isehemic postconditioning （LIPC） group. Rats were executed for cerebral tissues at 6, 12, 24, 48 and 72 h after operation, 8 in each time point, neuropathology, p63 expression, neuronal density and apoptosis were evaluated in hippocampus CA1 area. Results The positive rate of the cells expressing p63 in I/R group significantly higher than that in Sham group at the same time point （P 〈0. 01 ） , the rate of 48 h was higher than that of 24 h and 72 h, with statisti- cal significance （P 〈 0. 05 ）. The rate in LIPC group was significantly lower than that in I/R group （P 〈 0. 05 ）. Apoptotic index at 24 h, 48 h and 72 h after operation in I/R group was significantly increased than that in the Sham group （ P 〈 0. 05 ） , with maximum at 48 h. In LIPC group, apoptotic index was significantly decreased at the same time point than that in I/R group （P 〈 0. 05 ）, but higher than that in Sham group （P 〈 0. 05 ）. Conclusions The expression of p63 in cerebral ischemia/reperfusion shows a decreasing trend after the first increase, and neuronal apoptosis is basically the same, suggesting that p63 may be involved in neuronal apoptosis. LIPC plays a role in neuroprotection, and its mechanism could include reducin~ expression of o63 and inhibiting neuronal at3ootosis.

关 键 词：脑缺血 神经元凋亡 缺血后处理 P63 

分 类 号：R743.31[医药卫生—神经病学与精神病学] R-33[医药卫生—临床医学]