【摘要】 目的　探讨外伤性眼球萎缩眼视神经组织中 bcl- 2相关死亡基因 bad表达情况及其意义。　方法　用免疫组织化学的方法观察 8只正常对照尸体眼、31只外伤性眼球萎缩眼视神经组织中 bad的表达情况。　结果　眼球萎缩眼视神经退行性变表现为视神经髓鞘进行性脱失 ,神经胶质细胞增生补充。bad表达于正常视神经髓鞘组织及眼球萎缩眼视神经残存髓鞘组织 ,束间隔及神经胶质细胞中无 bad表达。眼球萎缩眼残存的视神经组织较正常视神经组织 bad表达量有增高趋势 (P<0 .0 5 ) ;但与眼球萎缩病程长短及导致眼球萎缩的病因之间无直接线性关系 (P>0 .0 5 )。　结论　 bad可能具有促进外伤性眼球萎缩眼视神经退行性变的作用更多还原

【Abstract】 Objective To study the expression and its significance of bcl-2 associated death (bad) gene in human optic nerves from traumatic atrophic eyeballs. Methods The optic nerves from 8 normal human donor eyes and 31 traumatic atrophic eyes were studied by immunohistochemistry technique. Results Bad protein was positively expressed in the normal optic nerve myelin sheath and residual myelin portions of optic nerve tissues from traumatic atrophic eyes. The expression of bad protein in the residual portions of myelin sheath was stained significantly stronger than that in normal optic nerves (P<0 05)? The pathological durations for ocular atrophy was not co-related with the quantites of expression of bad protein. There was no significant difference between pathogenic causes of ocular atrophies and the quantites of bad expression (P>0 05). Conclusion Bad might possess the function of promoting the optic nerve atrophy processes in traumatic atrophic eyes.更多还原