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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
Objective To investigate the expression of bcl-2-related death genes in traumatic atrophic orbital optic nerve and its significance. Methods Immunohistochemical method was used to observe the expression of bad in eight normal control cadaver eyes and 31 traumatic atrophic orbital optic nerves. Results Eye atrophy Optic neurodegeneration showed optic nerve myelin progressive loss, glial cell proliferation supplement. bad expression in normal optic nerve myelin sheath and ocular atrophic optic nerve remnant myelin tissue, beam interval and glial cells without bad expression. There was no significant linear relationship between the atrophic orbital atrophy and the atrophy of the optic atrophy (P <0.05) 5). Conclusion bad may have to promote traumatic atrophy of the optic nerve degeneration