视神经损伤后视网膜神经节细胞中肿瘤坏死因子在视神经管减压术后和药物干预的免疫活性研究

发布时间：2018-04-29 08:58

本文选题：视神经损伤 + 地塞米松　；参考：《新疆医科大学》2012年硕士论文

【摘要】：目的：探讨急性视神经损伤后经翼点入路视神经管减压术以及应用地塞米松药物治疗对兔视网膜神经节细胞（RGC）的凋亡过程干预作用及两种处理方案对视网膜神经节细胞中肿瘤坏死因子免疫活性的影响。方法：96只新西兰兔均建立右眼外伤性视神经损伤模型，左眼作为空白对照。所有动物模型按完全随机方法分为手术组，地塞米松组，损伤组，每组24只。按损伤后3、7、14、21天4个时间点，每组又分为4个小组，每小组8只。手术小组在急性视神经损伤模型建立后24h-48h间全麻下施行经翼点入路视神经管减压术；地塞米松小组在视神经损伤模型建立后持续给予地塞米松（1mg/kg，一日一次）。于损伤后第3、7、14、21天分别按随机原则处死相应天数手术小组、地塞米松小组，损伤小组动物模型，取材后分别行视网膜组织HE染色和TUNEL染色，光镜下对各小组视网膜神经节细胞进行计数并采用酶联免疫吸附试验（ELISA）检测TNF-浓度。结果：（1）随损伤后时间延长，损伤小组视网膜神经节细胞数逐渐减少，且在各时间点存活视网膜神经节细胞数存在差异并具有统计学意义；在各时间点手术小组与损伤小组的存活视网膜神经节细胞数存在差异并具有统计学意义；各时间点地塞米松小组与损伤小组的存活视网膜神经节细胞数存在差异并具有统计学意义。（2）手术小组在早期（3d、7d）的存活视网膜神经节细胞数明显高于地塞米松小组，差异具有统计学意义；手术小组在中晚期（14d、21d）的存活视网膜神经节细胞数略高于地塞米松小组，差异无统计学意义。（3）在不同的时间点手术小组TNF-α浓度均明显低于损伤小组并具有统计学意义；不同的时间点地塞米松小组TNF-α浓度均明显低于损伤小组并具有统计学意义。（4）在早中期（3d、7d、14d）时间点手术小组TNF-α浓度均明显低于地塞米松小组并具有统计学意义；但在晚期（21d）手术小组与地塞米松小组两组无明显差异，，无统计学意义。结论：急性视神经损伤后RGC凋亡是一个持续的细胞凋亡过程。经翼点入路视神经管减压术治疗对急性视神经损伤后RGC具有保护作用。视神经损伤后持续应用地塞米松对RGC具有保护作用。经翼点入路视神经管减压术治疗和应用地塞米松可减轻急性视神经损伤后TNF-α浓度的急性升高。
[Abstract]:Objective: to investigate the effect of decompression of optic canal via pterygoid approach and dexamethasone drug therapy on apoptosis of retinal ganglion cells in rabbits after acute optic nerve injury. Effect of tumor necrosis factor on immune activity in ganglion cells. Methods the traumatic optic nerve injury model of right eye was established in 96 New Zealand rabbits, and the left eye was used as blank control. All animal models were randomly divided into operation group, dexamethasone group and injury group with 24 rats in each group. Each group was divided into 4 groups with 8 rats in each group. After the establishment of the model of acute optic nerve injury, the operative group underwent tranpterional approach optic canal decompression under general anesthesia between 24h-48h, and the dexamethasone group was continuously given dexamethasone 1 mg / kg once a day after the establishment of the optic nerve injury model. On the 21st day after injury, the corresponding days of operation group, dexamethasone group and injury group were sacrificed according to random principle. The retinal tissues were stained with HE and TUNEL respectively. Retinal ganglion cells were counted under light microscope and TNF- concentration was detected by Elisa. Results the number of retinal ganglion cells in the injured group decreased gradually with the extension of the time after injury, and the number of retinal ganglion cells survived at each time point was different and had statistical significance. There were significant differences in the number of viable retinal ganglion cells between the operative group and the injured group at each time point. The number of viable retinal ganglion cells in the dexamethasone group and the injured group was significantly higher than that in the dexamethasone group. The number of viable retinal ganglion cells in the surgical group was slightly higher than that in the dexamethasone group. There was no significant difference in TNF- 伪 concentration between the two groups at different time points, and the TNF- 伪 concentration was significantly lower in the operation group than in the injury group. The concentration of TNF- 伪 in the dexamethasone group was significantly lower than that in the injury group at different time points (P < 0.05). The concentration of TNF- 伪 in the operation group was significantly lower than that in the dexamethasone group at the early and middle stage. However, there was no significant difference between the operative group and dexamethasone group at the late stage of 21 d. Conclusion: RGC apoptosis is a continuous process of apoptosis after acute optic nerve injury. Tranpterional approach to decompression of optic canal has protective effect on RGC after acute optic nerve injury. Continuous application of dexamethasone after optic nerve injury has protective effect on RGC. The treatment and application of dexamethasone through pterional approach to decompression of optic canal can reduce the acute increase of TNF- 伪 concentration after acute optic nerve injury.
【学位授予单位】：新疆医科大学
【学位级别】：硕士
【学位授予年份】：2012
【分类号】：R779.1

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