期刊文献+

急性颅脑损伤和神经元凋亡(英文)

Acute brain injuries and neuronal apoptosis
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摘要 目的:急性颅脑损伤是否存在神经元凋亡一直存在争议,主要原因是缺乏人脑损伤的直接资料来证实这一现象。文章简要综述凋亡的研究进展及急性颅脑损伤和神经元凋亡的关系。资料来源:应用计算机检索Medline数据库1995-01/2005-02相关文章,检索词为“Acute brain injuries”,“Neuronal apoptosis”,分别组合进行检索,限定文章语言种类为英语。同时计算机检索中国期刊全文数据库、万方数据库2000-01/2004-12期间的相关文章,检索词“急性颅脑损伤,神经元凋亡”,限定文章种类为中文。资料选择:对资料进行初审,选取急性颅脑损伤和神经元凋亡的随机和非随机对照实验。排除综述类和重复的文章。资料提炼:共收集到136篇关于急性颅脑损伤和神经元凋亡有直接关系的文章,其中有19篇符合标准,排除117篇。排除的117篇系重复或者与本文关系不大。资料综合:对检索到的文章的相关信息综合加以概括综述,总结出凋亡的相关因素、凋亡网络理论、凋亡的检测方法、急性颅脑损伤和神经元凋亡的关系及机制。结论:急性颅脑损伤后存在神经元凋亡;急性脑损伤后,神经元生存的内外环境发生了变化,各种因素如细胞外兴奋性氨基酸浓度升高、自由基的大量产生,基因表达的异常等相互交织,有可能存在多条通路调节神经元凋亡。 OBJECTIVE: Controversy over the presence of neuronal apoptosis in acute brain injuries has not been resolved due to the lack of direct evidence. In this article, the authors briefly review the current research progress of apoptosis and discuss the relationship between acute brain injuries and neuronal apoptosis.DATA SOURCES: A computer-based retrieval for relevant papers with abstracts indexed in Medline database published in English full text between January 1995 and February 2005 was conducted using the key words of “acute brain injuries” and “Neuronal apoptosis”. Related articles in Chinese full text published between January 2000 and December 2004 were also searched in Chinese periodical full text database, Wanfang databases with key words of “acute traumatic brain injury, neuronal apoptosis”.STUDY SELECTION: The retrieved articles were first examined to exclude review articles and repetitions, and only randomized and non-randomized controlled experiments or clinical trials on acute traumatic brain injury and neuronal apoptosis were included.DATA EXTRACTION: Altogether 136 articles directly related to acute traumatic brain injury and neuronal apoptosis were collected, among which 19 met the inclusion criteria with the other 117 removed for repetition or irrelevancy.DATA SYNTHESIS: The valid articles were reviewed to identify the factors related to neuronal apoptosis, apoptotic network theory, detection methods of apoptosis, and the relationship between acute traumatic brain injury and neuronal apoptosis as well as the possible mechanisms.CONCLUSION: Neuronal apoptosis occurs after acute traumatic brain injury, which induces intrinsic and extrinsic neuronal environment changes including increased extracellular excitatory amino acid content, massive free radical production and abnormal gene expression. These factors interact with each other and modulate neuronal apoptosis through multiple pathways.
作者 刘娜 孙志扬
出处 《中国临床康复》 CSCD 北大核心 2005年第41期190-192,共3页 Chinese Journal of Clinical Rehabilitation
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参考文献19

  • 1Parker JE, Mufti GJ.The role of apoptosis in the pathogenesis of the myelodysplastic syndromes.Int JHematol 2001;73(4):416-28
  • 2鲍刚,郭宁,张仲林,陈伟.大鼠脑出血模型中神经细胞凋亡的特征及Bcl-2蛋白对细胞凋亡的调控[J].中国临床康复,2004,8(31):6926-6927. 被引量:5
  • 3Schendel SL, Xie Z, Montal MO,et al. Channel formation by antiapoptotic protein Bcl-2.Proc Natl Acad Sci U S A 1997;94(10):5113-8
  • 4Susin SA, Lorenzo HK, Zamzami N, et al. Molecular. characterization of mitochondrial apoptosis-inducing factor. Nature 1999;397(6718):441-6
  • 5Li H, Zhu H, Xu CJ,et al. Cleavage of BID by caspase 8 mediates the mitochondrialdamage in the Fas pathway of apoptosis. Cell 1998;94(4):491-501
  • 6Cosulich SC, Savory PJ, Clarke PR.Bcl-2 regulates amplification of caspase activation by cytochrome c. Curr Biol 1999;9(3):147-50
  • 7Shimizu S, Narita M, Tsujimoto Y.Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC.Nature 1999;399(6735):483-7
  • 8Naumovski L, Cleary ML.The p53-binding protein 53BP2 also interacts with Bc12 and impedes cell cycle progression at G2/M.Mol Cell Biol 1996;16(7):3884-92
  • 9Wang HG, Rapp UR, Reed JC.Bcl-2 targets the protein kinase Raf-1 to mitochondria. Cell 1996;87(4):629-38
  • 10Johnson DE.Programmed cell death regulation: basic mechanisms and therapeutic opportunities. Leukemia 2000;14(8):1340-4

二级参考文献21

  • 1[1]Matsushita K, Matsuyama T, Kitagawa K, et al. Alterations of Bcl-2 family proteins precede cytoskeletal proteolysis in the penumbra, but not in infarct centres following focal cerebral ischemia in mice. Neuroscience 1998; 83 (2):439 -48
  • 2[2]Kitagawa K, Matsumoto M, Tagaya M, et al. Ischemic tolerance' phenomenon found in the brain. Brain Res 1990; 528(1): 21 -4
  • 3[6]Lotem J, Sachs L. Regulation by bcl-2, c-myc, and p53 of susceptibility to induction of apoptoais by heat shock and cancer chemotherapy compounds in differentiation-competent and -defective myeloid leukemic cells. Cell Growth Differ 1993; 4(1):41 -7
  • 4[7]Zhu Y, Prehn J, Culmsee C, et al. The beta 2-adrenoceptor agonist clenbuterol modulates Bcl-2, Bcl-xl and Bax protein expression following transient forebrain ischemia. Neuroscience 1999; 90(4): 1255 - 63
  • 5[8]Kluck RM, Bossy-Wetzel E, Green DR, et al. The release of cytochrome c from mitochondria: a primary site for Bcl-2 regulation of apoptosis. Science 1997; 21;275(5303): 1132 -6
  • 6[9]Takei N, Endo Y. Ca2 + ionophore-induced apoptosis on cultured embryonic rat cortical neurons. Brain Res 1994; 652 ( 1 ): 65 - 70
  • 7[10]Bellomo G, Perotti M, Taddei F, et al. Tumor necrosis factor alpha induces apoptosis in mammary adenocarcinoma cells by an increase in intranuclear free Ca2 +concentration and DNA fragmentation. Cancer Res 1992; 52(5): 1342 -6
  • 8[11]Hockenbery DM, Oltvai ZN, Yin XM, et al. Bcl-2 functions in an antioxidant pathway to prevent apoptosis. Cell 1993; 75(2): 241 - 51
  • 9[12]Crumrine RC, Thomas AL, Morgan PF, et al. Attenuation of p53 expression protects against focal is chemic damage in transgnic mice. Cereb Blood Flow Metab 1994: 14(12): 887 -91
  • 10[13]Yakovlev AG, Knoblaeh SM, Fan L, et al. Activation of CPP32-1ike caspases contributes to neuronal apoptosis and neurological dysfunction after traumatic brain injury. Neurosci 1997; 17 (19): 7415 - 24

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