天津医药

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大鼠外伤性视神经损伤后促凋亡基因P53、Bax和Caspase 3蛋白的表达

吕瀛娟1,颜华2,王世忠3,赵秀兰4   

  1. 1. 天津医科大学眼科中心
    2. 总医院眼科
    3. 天津医大组胚教研室
    4.
  • 收稿日期:2010-04-30 修回日期:2010-08-31 出版日期:2010-11-15 发布日期:2010-11-15
  • 通讯作者: 吕瀛娟

Expression of pro-apoptotic protein P53、Bax and caspase3 after traumatic optic nerve injury in rats

  • Received:2010-04-30 Revised:2010-08-31 Published:2010-11-15 Online:2010-11-15

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摘要： 目的：观察大鼠外伤性视神经损伤后不同时间点的视网膜神经节细胞(retinal ganglion cells，RGCs)病理形态学改变，及P53、Bax和Caspase3蛋白表达变化规律，探讨外伤性视神经损伤发生机制及促凋亡基因的作用。方法：应用液压颅脑损伤仪建立大鼠视神经损伤动物模型，伤后1，3，5，7，9，14，28天处死，病理学观察RGCs的改变，免疫组化方法分析P53、Bax和Caspase 3在视网膜中的表达变化。结果：视神经损伤后l天RGCs开始减少，7天内呈快速减少，14天后减少速度减慢，28天后趋于稳定；P53、Bax、Caspase 3伤后表达明显增加，与对照组表达水平相比，差异具有统计学意义(P<0.05)。结论：视神经损伤后RGCs数目减少是其视功能下降的重要病理基础，凋亡是RGCs的死亡机制之一，促凋亡基因P53、Bax和Caspase3在RGCs凋亡发生中起重要作用。

关键词: 外伤性视神经损伤, 促凋亡基因, P53, Bax, caspase3

Abstract: Objective: To explore the retinal ganglion cells (RGCs) pathological changes and expression of Bax, P53 and caspase3 protein in RGCs after the damage of the traumatic optic nerve injury in rats at different time points, to investigate the mechanism of traumatic optic nerve injury and the role of pro-apoptotic genes. Methods: the animal model of optic nerve injury in rats was built by fluid percussion brain injury device (FPI). Rats were killed on 1,3,5,7,9,14,28 days after injury. The changes of RGCs were observed by histopathology, the expression of Bax, P53 and caspase3 in RGCs were studied by immunohistochemistry method. Results: On the first day after the optic nerve injury the number of RGCs reduced. On the seventh day after the injury the number of RGCs decreased rapidly. On the fourteenth day after the injury the number of RGCs decreased slowly. On the twenty eighth day after the injury the number of RGCs stabilized. Expression of P53, Bax and Caspase3 mRNA increased in RGCs after the injury. The expression of those increased more significantly in the injury group than in control group (P<0.05). Conclusion: The decrease in the number of RGCs after the optic nerve injury is an important pathological basis in the degression of visual function. Apoptosis is one of the mechanisms of the death of RGCs. The pro-apoptotic protein P53, Bax and Caspase3 play an important role in RGCs apoptosis .

Key words: traumatic optic nerve injury, pro-apoptotic gene, P53, Bax, caspase3