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大鼠脑缺血再灌流后Bcl-2、Caspase-3 mRNA水平表达与大脑皮层及纹状体区炎性细胞浸润的影响 被引量:13

The Level Expression of Bcl-2 and Caspase-3 mRNA and Influence of the Relationship of the Infiltration of Inflammation Cells and in Cerebral Cortex and in Corpus Striatum Region after Cerebral Ischemia Reperfussion in Rats
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摘要 目的 探讨大鼠脑缺血再灌流后Bcl- 2蛋白、Caspase - 3mRNA的表达及炎性细胞浸润与神经细胞凋亡的关系。方法 将 5 4只Wistar大鼠随机分为二组 :假手术组 ,缺血再灌流组。采用原位末端标记 (TUNEL)、免疫组化和原位杂交技术分别观察脑缺血再灌流后不同时间点神经细胞凋亡及损伤的变化与Bcl- 2、Caspase - 3mRNA表达。 结果 Bcl- 2表达于缺血再灌流 12~ 2 4h达高峰 ,再灌流 2~ 4d呈下降趋势 ,至 16d略高于假手术组 ;Caspase- 3mRNA于缺血再灌流 12~ 2 4h达高峰 ,2~ 4d呈降低趋势 ,至 16d略高于假手术组。结论 脑缺血再灌流后细胞凋亡介导神经细胞损伤、坏死是一个渐进的动态演变过程。Bcl- 2蛋白、Caspase- Objective To explore relationship of the expression of Bcl-2 protein and Caspase-3 mRNA and the infiltration of inflammation cells and the neuron apoptosis after cerebral ischemia reperfussion in rats. Methods 54 rats were divided randomly into two groups: sham-operative group and ischemia reperfusion group. The variations of neuron apoptosis and neuron injury on the different time points after cerebral ischemia reperfussion in rats were observed with the method of deoxynucleotidy 1 tranferase mediated dUTP-flourescein nick end-labelig (TUNEL) assay. The expression of Bcl-2 protein with the method of immunchiochemistry and the expression of Caspase-3 mRNA with the method of in situ hybridization. Results It showed that expression of Bcl-2 protein reached a peak at 12~ 24h after reperfussion and begin to decrease at 2~4d .but the numbers of the positive cells were still in high level after 16d compared with the sham-operated group, The expression of Caspase-3 mRNA reached a peak at 12~24h after reperfusion and decreased at 2~4d, but the number of the positive cells was still in high level after 16d compared with the sham-operated group. Conclusions The neuron apoptosis guide in injury and necrosis was a dynamic ongoing development process after cerebral ischemia reperfussion in rats. The expression of Bcl-2 protein should inhibit apoptosis, Caspase-3 mRNA should guide in neuron injury play an very important role.
出处 《神经疾病与精神卫生》 2004年第4期252-255,共4页 Journal of Neuroscience and Mental Health
关键词 大鼠 脑缺血再灌流 BCL-2 CASPASE-3MRNA 大脑皮层 纹状体 炎性细胞 细胞凋亡 Iischemia reperfusion Neuron apoptosis Infiltration of inflammation cells Bcl-2 proleins Caspase-3 mRNA
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  • 1Buemi M,Allegr A,Aloisi C,et al.Cold pressor testraises serum concerntrations of ICAM - 1 v CAM - 1, and E - seletin in normotensive and hypertensive patients[].Journal of Hypertension.1997
  • 2Longa EL.Reversible middle cerebral artery occlusion without cranietomy in rats[].Stroke.1998
  • 3Marlangue CC,Margaill I,Represa A,et al.Apoptosis and necrosis after reversible focal ischemia: an in situ DNA fragmentation analysis[].Journal of Cerebral Blood Flow and Metabolism.1996
  • 4Block F,Peters M,Nolden-Koch M.Expression of IL-6 in the ischemic pneumbra[].Neuroscience Letters.1999
  • 5Wechenberger M,Mendoza LH,Youker KA.Cardiac myocytes produce interleukin- 6 in culture and in viable border zone of reperfused infarctions[].Circulation.1999
  • 6Lawrence Ms,Ho D Y,Sun G H,et al.Overexpression of Bcl2 with herpes simplex virus vectors protects CNS neurons against neurological insults in vitre and vivo[].Neuroscience.1996
  • 7Srinivasula SM,Fernandes-Alnemri T,Zangrilli J,et al.The ced- 3/ interleukin 1 beta converting enzyme - like homolog Mch6 and the lamincleaving enzyme Mch2 alpha are substrates for the apoptotic mediator cpp32[].Journal of Biological Chemistry.1996
  • 8N i B,W u X,Su Y,et al.Transient global forebrain ischem ia in-duces a prolonged expression of the caspase-3 mRNA in rat h ipp-ocampal CA1 pyram idal neurons[].Cereb B lood Flow M etab.1998
  • 9Namura S,Zhu J,Fink K,et al.Activation and cleavage of caspase - 3 in apoptosis induced by experimental cerebral ischemia[].Neuroscience.1998
  • 10Zhu C,Wang X,Hagberg NL,et al.Correlation between caspase- 3 activation and three different markers of DNA damage in neonatal cerebral hypoxia - ischemia[].Neurochemistry International.2000

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