| 吴昊昊,丁昕,徐美玲,戴培文,张军军,冀胜军,田野.电离辐射对大鼠海马区神经发生及TrkA和TrkB表达的影响[J].中华放射医学与防护杂志,2017,37(4):241-245 |
| 电离辐射对大鼠海马区神经发生及TrkA和TrkB表达的影响 |
| The role of TrkA/TrkB in radiation-induced hippocampal neurogenesis impairment |
| 投稿时间：2016-11-01 |
| DOI：10.3760/cma.j.issn.0254-5098.2017.04.001 |
| 中文关键词: 电离辐射 神经发生 TrkA蛋白 TrkB蛋白 |
| 英文关键词:Ionizing radiation Neurogenesis TrkA TrkB |
| 基金项目:国家青年科学基金（81402517）；国家自然科学基金（81372411，81172128）；江苏省临床医学科技专项（BL2014040）；江苏省青年医学人才基金（QNRC2016234） |
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| 中文摘要: |
| 目的 探讨电离辐射对大鼠海马区神经发生以及TrkA、TrkB蛋白表达的影响。方法 将56只SD大鼠按随机数字表法分为照射组（28只）和健康对照组（28只），照射组给予单次10 Gy全脑照射。分别于照后1、3 d，2周以及1个月取海马组织，应用免疫荧光染色观察神经元增殖变化，Golgi染色观察海马树突棘形态变化，Western blot及RT-PCR分别检测TrkA、TrkB蛋白及RNA水平变化。结果 与健康对照组比较，免疫荧光染色显示照射组双皮质素（DCX）数量明显减少（t=6.49，P<0.05）。照射组海马树突棘明显减少，且树突棘的形态变化明显。与健康对照组相比，照后不同时间照射组TrkA蛋白表达明显升高（t=2.64、3.06、4.80、2.64， P<0.05），而TrkB的表达则显著下降（t=4.59、3.06、2.81、2.57， P<0.05）；TrkA mRNA表达水平明显升高（t=4.57、3.06、5.39、5.86， P<0.05），TrkB的表达显著下降（t=14.87、11.69、4.98，P<0.05）。结论 作为神经生长因子、脑源性神经因子重要的下游信号通路分子，全脑照射后TrkA、TrkB的表达变化，可能在电离辐射所致海马神经发生损伤中发挥重要作用。 |
| 英文摘要: |
| Objective To investigate the roles of TrkA and TrkB in radiation-induced hippocampal neurogenesis impairment.Methods Fifty-six rats were randomized into radiation group and sham control group. Radiation group received whole brain irradiation at a single dose of 10 Gy. The hippocampus were separated from rats in day 1, day 3, day 14 and 1 month after irradiation. Western blot and RT-PCR were applied to detect the protein levels and mRNA levels. Golgi staining was used to observe the dendritic spine of hippocampus. Immunofluorescence was performed to detect neural precursor's proliferation. Results Compared with control group, the numbers of dendritic spine significantly decreased after irradiation and its shape change obviously. Immunofluorescence showed a significant decrease in neural precursor's proliferation comparing with control group (t=6.49, P<0.05). Protein level of TrkA expression increased (t=2.64, 3.06, 4.80, 2.64, P<0.05), while the levels of TrkB protein expression decreased significantly (t=4.59, 3.06, 2.81, 2.57, P<0.05).The mRNA level of TrkA expressions increased (t=4.57, 3.06, 5.39, 5.86, P<0.05), while the mRNA level of TrkB decreased (t=14.87, 11.69, 4.98, P<0.05). Conclusions As a signaling pathways downstream of NGF and BDNF, TrkA and TrkB may play an important role in radiation-induced neurogenesis impairment. |
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