辐射诱导发育脑细胞凋亡的分子调节

古桂雄

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辐射诱导发育脑细胞凋亡的分子调节

    作者简介: 古桂雄(1954-),男,广东兴宁人,苏州医学院儿童医院主任医师,博士,主要从事发育脑保护的研究。;
  • 中图分类号: Q274

Influence of radiation-induced apoptosis on development brain in molecular regulation

  • CLC number: Q274

  • 摘要: 近年来辐射诱导脑细胞损伤研究表明,某些基因如即早基因、Bcl-2家族、P53热休克蛋白、AT(共济失调性毛细管扩张症)基因电脑辐射放育的细胞凋亡中发挥重要的调控作用;而神经生长因子、白细胞介素-l、肿瘤坏死因子、碱性纤维生长因子、转化生长因子等生物因子在抑制辐射诱导细胞凋亡中具有重要的保护作用。
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    [3] Ferrer I,Olive M,Ribera J,et al.Naturally occurring (programmed) and radiation-induced apoptosis are associated with selective c-Jun expression in the developing rat brain[J]. Eur J Neurosci, 1996, 8(6):1286~1298.
    [4] Blank KR, Rudoltz MS, Kao GD, et al. The molecular regulation of apoptosis and implication for radiation oncology[J]. Int J Radiat Biol,1997, 71:455~466.
    [5] Borovitskaya AE, Evtushenko VI, Sabol SL. Gamma-radiation-induced cell death in the fetal rat brain possesses molecular characteristics of apoptosis and is associated with specific messenger RNA elevations[J]. Brain Res Mol Brain Res,1996, 35(1-2):19~30.
    [6] Kitada S,Krajewski S,Miyashita T,et al.Gamma-radiation induces upregulation of Bax protein and apoptosis in radiosensitive cells in vivo[J]. Oncogene,1996, 12(1):187~192.
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    [8] Wang X,Matsumoto H,Okaichi K,et al.p53 aoccumulation in various organs of rats after whole-body exposure to low-dose X-ray irradiation[J].Anticancer Res, 1996, 16(4A):1671~1674.
    [9] Wang B, Takeda H, Gao WM, et al. Induction of apoptosis by beta radiation from tritium compounds in mouse embryonic brain cells[J]. Health Phys, 1999,77(1):16~23.
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    [14] Raju U, Gumin GJ, Tofilon PJ. NF kappa B activity and target gene expression in the rat brain after one and two exposures to ionizing radiation[J]. Radiat Oncol Investig, 1999, 7(3):145~l52.
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  • 收稿日期:  1999-01-13

辐射诱导发育脑细胞凋亡的分子调节

    作者简介:古桂雄(1954-),男,广东兴宁人,苏州医学院儿童医院主任医师,博士,主要从事发育脑保护的研究。
  • 215003 江苏 苏州, 苏州医学院附属儿童医院

摘要: 近年来辐射诱导脑细胞损伤研究表明,某些基因如即早基因、Bcl-2家族、P53热休克蛋白、AT(共济失调性毛细管扩张症)基因电脑辐射放育的细胞凋亡中发挥重要的调控作用;而神经生长因子、白细胞介素-l、肿瘤坏死因子、碱性纤维生长因子、转化生长因子等生物因子在抑制辐射诱导细胞凋亡中具有重要的保护作用。

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