视明注射液对外伤性视神经萎缩的治疗作用及其机理的实验研究

【作者】 庞龙；

【导师】 王明芳；

【作者基本信息】 成都中医药大学 ， 中医眼科学， 2002， 博士

【摘要】 目的：探索并确立实验性外伤性视神经萎缩模型的建立方法；观察中药制剂视明注射液对外伤性视神经萎缩的治疗作用，并探讨其治疗作用的机理。 方法：采用改良的Klolein术式，在定量致伤的条件下建立实验性外伤性兔视神经萎缩模型，于20天和40天后分批作F-VER和病理形态学检查。再用同样的方法造模：40天后予视明注射液治疗，连续给药1个月后，作视觉电生理检查，取视神经作病理形态学、免疫组织化学检查，观察视明注射液对视神经的视觉电生理功能、轴浆运输、光镜及电镜下病理改变、视神经组织中大分子物质表达和微循环等方面的影响。 结果：改良的Klolein术式造模40天后，造模组兔眼视觉电生理的F-VER降低或丧失；神经纤维数量显著减少、脱髓鞘、神经胶质细胞增生。视明注射液改善了外伤性视神经萎缩兔眼视觉电生理的F-VER，增加了视神经纤维的数量，减轻了视神经纤维脱髓鞘，抑制了神经胶质细胞的增生；同时增加了视神经轴浆中辣根过氧化物酶反应颗粒积分光密度，抑制了视神经组织中ICAM-1表达，增加视神经组织中NT-3、CD34的表达和神经微丝蛋白的含量。 结论：采用改良的Klolein术式建立的实验性外伤性兔视神经萎缩模型是成功的。视明注射液能有效治疗外伤性视神经萎缩，其作用机理与促进轴浆运输、改善视神经纤维存活和再生的微环境和微循环、维护和构建视神经纤维的微结构有关。更多还原

【Abstract】 Objective: To establish an experimental animal mode! of opiic atrophy and then to determine the method of establishing this model. And then to investigate the effect and mechanism of Shiming Injection (a kind of preparation of Chinese medicine) on traumatic optic atrophy .Methods: In the first experiment , with a fixed amount of wound the rabbit model of traumatic optic atrophy(TOA) was established by reformative Klolein operation . after 20 and 40 days, all the studied rabbits were given the examinations of flash visual evoke response(F-VER) and pathomorphology . In the second experiment, 40 days after establishing TOA model by the same method , we given the TOA rabbits treatment with Shiming Injection for 30 days continuously . Then, we studied the effect of Shiming Injection on the visual function, axonal transport, pathologic changes, expression of some molecules and microcirculation of optic nerve by the examinations of F-VER, pathomorphology in light and electric scopes and immuncytochemisty.Results: In the visual function of optic nerve, F-VER was significantly lowered and the amount of optic nerve fiber was significantly decreased with a result of demyelination and neuroglia cell hyperplasia 40 days after establishing the TOA model. Shiming Injection improved F-VER, increased the amount of optic nerve fiber, alleviated pathological demyelination and inhibited hyperplasia of neurogiia cell. At the same time Shiming Injection accelerate the transportation of HorserAdish peroxidase (HRP) in axonal plasm and restrained the expression of ICAM-1. Additionally, Shiming Injection increased the expression of NT-3, CD34 and the content of neurofilament protein in optic nerve after treating with Shiming Injection for 30 days.Conclusion: About 40 days later, the experimental rabbit TOA model was established successfully by ligaturing optic nerve. Shiming Injection can treat experimental TOA efficiently by accelerating transportation of axonal plasm, improving the microenvironment and the microcirculation for optic nerve fiber to survive or regenerate and maintaining or rebuilding the microstructure of optic nerve fiber.更多还原