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青霉素致痫鼠脑组织中凋亡调控基因P^(53)及Bcl-2的表达及意义 被引量:7

Expression of P^(53) and Bcl-2 in hippocampus and cerebral cortex in penicillini-induced seizures in rats
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摘要 目的 探讨癫痫鼠脑组织中 P5 3及 Bcl-2的表达及意义。方法 通过免疫组化方法对青霉素致痫鼠癫痫灶脑组织中的 P5 3 、Bcl-2进行检测。结果 随着痫性发作次数的增多 ,P5 3 有显著的上升趋势 ;致痫组有 Bcl-2的表达 ,发作 8次组 Bcl-2表达最高 ,以后随着痫性发作次数的增多 ,有显著的下降趋势 ;P5 3 基因与 Bcl-2蛋白表达呈负相关性。结论  P5 3 基因表达水平与神经元损害程度有一定的关系。P5 3 基因可诱导 Bcl-2表达的减少 ,神经细胞的自我保护是有限的。 Objective To investigate the change of P 53 and Bcl 2 in cerebral tissues induced by seizures.Methods The model of seizure in Wistar rats was performed by injecting penicillini intraperitoneally.The levels of P 53 and Bcl 2 were detected by immunohistochemistry.Results (1)The level of P 53 in the epileptic group was significantly higher than that in the control group (P<0.01).The level of P 53 in the hippocampus is significantly higher than that in the cerebral cortex in the epileptic group (P<0.05).(2)There was no expression of Bcl 2 in the control group . There was expression of Bcl 2 in the epileptic group . The level of Bcl 2 in the hippocampus was significantly higher than that in the cerebral cortex (P<0.01). The level of Bcl 2 in the epileptic group with eight onsets was highest(P<0.01).(3)There was an inverse relationship between the expression of P 53 and that of Bcl 2.Conclusion Increased P 53 expression corrlates with the degree of neuronal injury . The change of Bcl 2 protein in the brain cells may protect the cells from injury and apoptosis. But the protection role of Bcl 2 is limited .Increase of P 53 expression may induce the decrease of Bcl 2 expression.
出处 《中风与神经疾病杂志》 CAS CSCD 北大核心 2001年第4期220-222,共3页 Journal of Apoplexy and Nervous Diseases
关键词 癫痫 细胞凋亡 P^53 BCL-2 免疫组织化学 青霉素 Epilepsy Apoptosis P 53 Bcl 2 Immunohistochemistry
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  • 1Hua S Y,Endocrinology,1989年,124卷,687页
  • 2陈启贤,华西医科大学学报,1987年,18卷,11页
  • 3唐竹吾,中枢神经系统解剖学,1986年

共引文献11

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  • 1杜新鲁,高慧明,赵杰,刘学源,张万琴.癫痫发作敏感大鼠T区κ型阿片受体和NR_(2B)表达变化[J].神经解剖学杂志,2004,20(5):463-467. 被引量:2
  • 2方瑗,童萼塘,孙圣刚,梅元武,曹非.鼠脑缺血后神经元凋亡与P53的关系及碱性成纤维细胞生长因子的影响[J].中华老年心脑血管病杂志,2000,2(3):196-199. 被引量:1
  • 3李震中,阮旭中,王群,张苏明.BCL—2蛋白在癫痫过程中海马细胞内的变化[J].脑与神经疾病杂志,1996,4(2):71-73. 被引量:8
  • 4[1]吴逊.神经病学:癫痫与发作性疾病.北京:人民军医出版社,2001:171-172.
  • 5[2]Bengzon J,Mohapel P,Ekdahl CT,et al.Neuronal apoptosis after brief and prolonged seizures.Prog Brain Res,2002,135:111-119.
  • 6[3]Uysal H,Cevik IU,Soylemezoglu F,et al.Is the cell death in mesial temporal scelrosis apoptotic.Epilepsia,2003,44:778-784.
  • 7[4]Schon EA,Manfredi G.Neuronal degeneration and mitochondrial dysfunction.J Clin Invest,2003,111:303-312.
  • 8[5]Adams JM,Corys.The Bcl-2 protein family:arbiters of cell survival.Science,1998,281:1322-1326.
  • 9[6]Henshall DC,Clark RS,Adelson PD,et al.Alterations in bcl-2 and caspase gene family expression in human temporal lobe epilepsy.Neurology,2000,55:250-257.
  • 10[7]Yi X,Yin XM,Dong Z.Inhibition of bid-induced apoptosis by bcl-2:tbid insertion,bax translocation and bax/bak oligomefization suprressed Biol Chem,2003,278:16992-16999.

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