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目的建立眶内视神经慢性受压损伤动物模型,并观察睫状神经营养因子(CNTF)和生长相关蛋白-43(GAP-43)在视神经中的表达。设计实验研究。研究对象新西兰大白兔36只。方法将动物分为6组,即A组(无压迫组):只放置球囊而不充盈造影剂;B组(2w):逐量注入造影剂压迫2周;C组(2w+2w):压迫2周后解除压迫2周;D组(4w):注入造影剂压迫4周;E组(4w+4w):压迫4周解除压迫4周;F组(8w):压迫8周。用眼眶内植入气囊并定时注入造影剂的方法 ,模拟眼眶肿瘤缓慢生长对眶内视神经慢性压迫,建立视神经慢性损伤动物模型;用RT-PCR方法检测在眶内视神经慢性损伤后不同阶段(造模后2、4、8周)CNTF和GAP-43的基因表达。主要指标CNTF和GAP-43的表达。结果眼底像和组织病理检查显示,随着压迫时间的延长,眼底、视网膜和视神经都出现病理改变并逐渐加重。空白及无压迫组低表达CNTF和GAP-43,压迫2周后即可见表达上调(P<0.01),随着压迫时间延长,两种基因均见表达逐渐增高(P<0.01)。结论成功建立兔眶内视神经慢性损伤动物模型,并观察到随着压迫时间的延长,CNTF和GAP-43在视神经中的表达量逐渐增多,提示神经细胞被外来损伤诱导,开始进行自身修复。
Objective To establish a chronic compression injury model of orbital optic nerve in rats and observe the expression of ciliary neurotrophic factor (CNTF) and growth associated protein-43 (GAP-43) in optic nerve. Design experiment research. Study New Zealand white rabbits 36. Methods The animals were divided into 6 groups: group A (no compression group): balloon only without filling contrast agent; group B (2w) Group D (4w): 4 weeks after injection of contrast agent; Group E (4w + 4w): 4 weeks after compression and 4 weeks after compression; Group F (8w): 8 weeks after compression. The intraocular orbital implanted balloon and timed injection of contrast agent were used to simulate the chronic growth of orbital optic nerve chronic orbital oppression of chronic optic nerve, the establishment of chronic optic nerve damage in animal models; RT-PCR method in orbital optic nerve after chronic injury at different stages 2, 4, 8 weeks after mold) gene expression of CNTF and GAP-43. The main indicators CNTF and GAP-43 expression. The results of fundus and histopathological examination showed that with the extension of oppression, the pathological changes of the fundus, retina and optic nerve appeared and gradually aggravated. The expressions of CNTF and GAP-43 were down-regulated in both blank and non-stressed groups, and were up-regulated after 2 weeks of compression (P <0.01). The expressions of both genes were increased with the prolongation of compression time (P <0.01). Conclusion The animal model of chronic orbital damage in the optic nerve was successfully established. It was observed that the expression of CNTF and GAP-43 in the optic nerve gradually increased with the prolonging of the compression time, which indicated that the nerve cells were induced by external injury and began to repair themselves.