摘要
目的:探讨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(RGCs)病理形态学改变,P53、Bax和Caspase3蛋白表达变化及其与视神经损伤发生机制的关系。方法:成年雌性Wistar大鼠72只,随机分9组,每组8只,其中2组分别为正常组和假伤组,其余为实验组。实验组应用液压颅脑损伤仪建立大鼠视神经损伤动物模型,分别于伤后1、3、5、7、9、14、28d各处死8只,病理学观察RGCs的改变,免疫组化方法分析P53、Bax和Caspase3在视网膜中的表达变化。结果:视神经损伤后ldRGCs开始减少,14d内呈快速减少,14d后减少速度减慢,28d后趋于稳定;P53、Bax、Caspase3伤后表达较正常组和假伤组明显增加。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,P53、Bax和Caspase3在RGCs凋亡发生中起重要作用。
Objective： To explore the pathological changes and expression of Bax, P53 and Caspase3 protein in retinal ganglion cells （RGCs） after the traumatic optic nerve injury in rats at different time points, and the mechanism of traumatic optic nerve injury thereof. Methods： Seventy-two adult female Wistar rats were used in this study. The rats were randomly divided into 9 groups,of which two groups were the control group （8 rats） and the sham group （8 rats）, the others were the experimental groups. The animal model of the optic nerve injury was built by fluid percussion brain injury device （FPI） in rats. Eight rats were killed 1, 3, 5, 7, 9, 14 and 28 days after injury. The pathological changes and the expressions of Bax, P53 and caspase 3 were observed in RGCs. Results： It was found that the number of RGCs reduced on the first day after the optic nerve injury. The number of RGCs decreased rapidly in 14 days after the injury, decreased slowly after 14 days of the injury, but it was stabilized after 28 days of the injury. Expressions of P53, Bax and Caspase3 mRNA were significantly increased in RGCs after the injury in the injury group than those in control group. Conclusion： The reduced number of RGCs after the optic nerve injury is an important pathological basis in the decline of visual function. Apoptosis is one of the mechanisms of the death of RGCs. The pro-apoptotic protein P53, Bax and caspase 3 play an important role in apoptosis of RGCs.
出处
《天津医药》
CAS
北大核心
2010年第11期996-998,1028,共4页
Tianjin Medical Journal
