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p63与大鼠全脑缺血后神经元凋亡的关系 被引量:1

Relationship between p63 and neuronal apoptosis after global cerebral ischemia in rats
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摘要 目的探讨p63与大鼠全脑缺血后神经元凋亡的关系。方法将80只SD大鼠随机分为两组(每组40只):假手术(Sham)组和全脑缺血/再灌注(I/R)组。两组分别在手术后6、12、24、48、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组术后24、48、72 h神经行为学评分较Sham组同时间点增高,差异有统计学意义(P<0.01),其中与同组24、72 h比较,术后48 h最高[(2.6±0.5)分],差异有统计学意义(P<0.05);I/R组海马CA1区p63阳性表达率在术后12、24、48、72 h较Sham组同时间点增高,差异有统计学意义(P<0.01),其中与同组12、24、72 h比较,术后48 h最高[(70.6±9.2)%],差异有统计学意义(P<0.01);细胞凋亡指数较Sham组增加,差异有统计学意义(P<0.01),其中与同组24、72 h比较,术后48 h最高,差异有统计学意义(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。 Objective To study the relationship between p63 and neuronal apoptosis after global cerebral ischemia in rats. Methods 80 male SD rats were randomly divided into two groups,40 cases in each group,the sham group and the global cerebral ischemia/reperfusion (I/R) group. Rats were executed for taking cerebral tissues at 6,12,24,48,72 h after operation, 8 cases in each time point. The neurobehavior scores were evaluted and p63 protein expression ,neuronal density and apoptosis in hippocampus CA 1 area were detected. Results The neurobehavior scores at postoperative 24,48,72 h in the I/R group were increased at the same time point compared with the the shamp group (P〈0.01), which at 48 h was highest, showing statistical difference. The positive expression rate p63 protein of hippocampus CA1 area at postoperative 12,24,48,72 h in the I/R group were significantly higher than that at the same time point in the sham group (P〈0.01), which at 48h was highest (P〈0.01), showing statistical difference. The cellular apoptosis index in the I/R group was significantly increased compared with the sham group(P〈0.01 ), showing statistical difference, maximum was at 48 h compared with that at 24,72 h in the same group, difference showing statistical significance (P〈0.05). Conclusion The expression of p63 in global cerebral ischemia/reperfusion shows the trend of decreasing firstly and then decreasing, which is basically consistent with neuronal apoptosis trend, suggesting that p63 may be involved in neuronal apoptosis.
出处 《现代医药卫生》 2012年第23期3525-3527,3530,共4页 Journal of Modern Medicine & Health
基金 四川省卫生厅科研基金资助项目(100289) 泸州市科技计划资助项目[2010S14(3-16)]
关键词 脑缺血 再灌注损伤 神经元 细胞凋亡 P63 Brain ischemia Reperfusion injury Neurons Apoptosis p63
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  • 1叶青山,马虹,王俊科,施伟忠,刘红,海克荣,韩洪伟,马聚峰,张岩.肝素预抗凝对窒息性心跳骤停大鼠心肺脑复苏效果的影响[J].中华麻醉学杂志,2007,27(5):459-462. 被引量:8
  • 2Longa EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral artery occlusion without craniectomy in rats[J]. Stroke, 1989,20 ( 1 ) :84-91.
  • 3贾海英,王继群,山艳春,王晓茜,唐智.p63及p53基因在喉鳞癌中的表达及意义[J].广东医学,2007,28(2):215-216. 被引量:4
  • 4Kato H, LiuY, Araki T, et al. Temporal profile of the effects of pretreat- ment with brief cerebral ischemia on the neuronal damage following sec- ondary isehemic insult in the gerbil : cumulative damage and protective ef- fects[J]. Brain Res, 1991,553 (2) : 238-242.
  • 5吕鹏,李玲,张丽.大鼠全脑缺血对再灌注海马区NO含量和Bcl-2表达的影响[J].大连医科大学学报,2009,31(6):649-652. 被引量:9
  • 6Zhang J, Qian H, Zhao P, et al. Rapid hypoxia preconditioning protects cortical neurons from glutamate toxicity through delta-opioid receptor[J]. Stroke, 2006,37 (4) : 1094-1099.
  • 7陈宏志,陈卫民.全脑缺血再灌注损伤中JNK及Bim蛋白的表达[J].中国现代医学杂志,2007,17(7):809-812. 被引量:14
  • 8Schmale H, Bamberger C. A novel protein with strong homology to the tu- mor suppressor p53[J]. Oncogene, 1997,15 (11 ) : 1363-1367.
  • 9Jaeobs WB, Govoni G, Ho D, et al. p63 is an essential proapoptotic protein during neural development[J]. Neuron, 2005,48 ( 5 ) : 743-756.
  • 10Bui T,Sequeira J ,Wen TC ,et al. ZEB1 links p63 and p73 in a novel neu- ronal survival pathway rapidly induced in response to cortical ischemia[J]. PLos One, 2009,4 (2) : e4373.

二级参考文献34

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同被引文献16

  • 1黄平,杨宇明,李德祥,李丽娟,张梅,张莹.甲状腺肿瘤p63、p16基因表达与细胞增殖活性的关系[J].临床与实验病理学杂志,2006,22(3):378-379. 被引量:7
  • 2刘斌,张强,张宇,张晋霞.脑缺血再灌注后不同时间点病理变化与细胞凋亡的研究[J].陕西医学杂志,2007,36(4):395-397. 被引量:17
  • 3Weir DL, Goodchild CS, Graham DI. Propofol : effects on indicesof cerebral ischemia [J]. J Neurosurg Anesthesiol,1989,1 (3):284-289.
  • 4Flores ER,Tsai KY, Crowley D,et al. p63 and p73 are requiredfor p53- dependent apoptosis in response to DNA damage[J]. Na-ture ,2002,416(6880):560-564.
  • 5Fujiki M,Hikawa T,Abe T,et al. Role of protein kinase C in ne-uroprotective effect of geranylgeranylacetone, a noninvasive in-ducing agent of heat shock protein,on delayed neuronal deathcaused by transient ischemia in rats[J]. J Neurotrauma, 2006,23(7):1164-1178.
  • 6Levy J,Zhu Z,Dunbar JC. The effect of global brain ischemia innormal and diabetic animals : the influence of calcium channelblockers[J].Endocrine,2004,25(2) :91-95.
  • 7Bates B,Hirt L,Thomas SS,et al. Neurotrophin-3 promotes celldeath induced in cerebral ischemia,oxygen-glucose deprivation,and oxidative stress : possible involvement of oxygen free radicals[J]. Neurobiol Dis,2002,9(1):24-37.
  • 8Chen M,Lu TJ,Chen XJ,et al. Differential roles of NMDA rece-ptor subtypes in ischemic neuronal cell death and ischemic toler-ance[J]. Stroke, 2008,39(11) :3042-3048.
  • 9Mronga T,Stahnke T,Goldbaum 0,et al. Mitochondrial pathwayis involved in hydrogen-peroxide-induced apoptotic cell death ofoligodendrocytes[J]. Glia,2004,46(4) ;446-455.
  • 10Jacobs WB,Govoni G, Ho D, et al. P63 is an essential proapop-totic protein during neural developmentfj]. Neuron,2005,48(5):743-756.

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