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BACKGROUND:The main clinical treatments for optic nerve injury are optic canal decompression and systemic administration of hormones,but both treatments have disadvantages.OBJECTIVE:To observe the pathological changes in the retina and growth associated protein-43(GAP-43) expression,to compare the treatment of optic canal decompression,hormones,and their combination with the intracanalicular optic nerve injury.DESIGN,TIME AND SETTING:A randomized,controlled animal study was performed at the Department of Anatomy,Weifang Medical University,China,from September 2007 to November 2008.MATERIALS:Dexamethasone(Shandong Huaxin Pharmaceutical,China) and rabbit anti-GAP-43 polyclonal antibody(Boster,China) were used.METHODS:All 36 healthy adult rabbits were randomly assigned to control group(n = 4),simple injury group(n = 20),and treatment group(n = 12).Intracanalicular optic nerve injury models were established using the metal cylinder free-fall impact method.The control group was left intact.The treatment group(four rabbits in each subgroup) was treated by optic nerve decompression,dexamethasone treatment(1 mg/kg daily via two intravenous infusions,1/5 total dose reduction every 3 days,for 14 days),and simultaneously giving surgery and hormone treatment.MAIN OUTCOME MEASURES:Pathological changes in the retina were determined using hematoxylin-eosin staining.GAP-43 expression was detected using immunohistochemistry in the retina.RESULTS:Retina injury induced obvious pathological changes in the retina.With prolonged time after optic nerve injury,the number of retinal ganglion cells was gradually decreased,and reached the minimum on day 14(P < 0.01).All three treatments increased the number of retinal ganglion cells(P < 0.01),but surgery + hormone treatment was most effective.No GAP-43 cells were present in the normal retinal,but they appeared 3 days after injury,peaked 7 days after injury,and then began to decline.CONCLUSION:Intracanalicular optic nerve injury induced obvious pathological changes in the retina,including increased GAP-43 expression.Optic canal decompression and hormones improved nerve repair after injury,and their combination produced better outcomes.
BACKGROUND: The main clinical treatments for optic nerve injury are optic canal decompression and systemic administration of hormones, but both treatment with hormones, but both treatments have hormones. OBJECTIVE: To observe the pathological changes in the retina and growth associated protein-43 (GAP-43) expression, to compare the treatment of optic canal decompression, hormones, and their combination with the intracanalicular optic nerve injury. DESIGN, TIME AND SETTING: A randomized, controlled animal study was performed at the Department of Anatomy, Weifang Medical University, China, from September 2007 to November 2008. Materals: Dexamethasone (Shandong Huaxin Pharmaceutical, China) and rabbit anti-GAP-43 polyclonal antibody (Boster, China) were used.METHODS: All 36 healthy adult rabbits randomly assigned to control group (n = 4) injury group (n = 20), and treatment group (n = 12). Intracanalicular optic nerve injury models were established using the metal cylinder free-fall impact method. The control group was left intact. The treatment group (four rabbits in each subgroup) was treated by optic nerve decompression, dexamethasone treatment (1 mg / kg daily via two intravenous infusions, 1/5 total dose reduction every 3 days, for 14 days), and simultaneously giving surgery and hormone treatment. MAIN OUTCOME MEASURES: Pathological changes in the retina were determined using hematoxylin-eosin staining. GAP-43 expression was detected using immunohistochemistry in the retina. RESULTS: Retina injury induced obvious pathological changes in the retina. Wilt prolonged time after optic nerve injury, the number of retinal ganglion cells was gradually decreased and reached the minimum on day 14 (P <0.01) .All three treatments increased the number of retinal ganglion cells (P <0.01), but surgery + hormone treatment was most effective. No GAP-43 cells were present in the normal retinal, but but 3 days after injury, peaked for 7 days after injury, and then began to decline. CONCLUSION: Intracanalicular optic nerve injury induced obvious pathological changes in the retina, including increased GAP-43 expression. Optic canal decompression and hormones improved nerve repair after injury, and their combination produce better outcomes.