丙戊酸钠在大鼠视神经损伤再生中的作用研究

目的 探讨丙戊酸钠在视神经损伤再生中的作用.方法 清洁级健康雄性SD大鼠60只,随机分3组：正常组12只（24只眼）、生理盐水对照组（对照组）和丙戊酸钠治疗组（治疗组）每组24只（24只眼）.正常组不做任何处理,两实验组均采用视神经钳夹法建立右眼视神经损伤模型,治疗组给予丙戊酸钠300 mg/kg腹腔注射,对照组给予等量生理盐水腹腔注射.分别于损伤后3d、7d、14 d、21 d取材,制备视网膜切片,光镜下观察视网膜神经节细胞（RGC）的病理形态学变化,以免疫组织化学技术观察脑源性神经营养因子（BDNF）的表达情况,计算机图像分析技术半定量检测视网膜组织BDNF的平均光密度值（AOD）.结果 与对照组比较,治疗组经丙戊酸钠注射后,视网膜神经节细胞水肿及空泡化程度轻,各层胞核排列相对密集整齐.相同时间点治疗组BDNF免疫组化染色的AOD值及阳性细胞计数均强于对照组和正常组.结论 丙戊酸钠可以促进视神经损伤后BDNF表达的上调,减少RGC的损伤,对视神经损伤具有保护作用.

The role of Sodium valproate in the regeneration of injured optic nerve in rats

Objective To study the role of Sodium valproate in the regeneration of injured optic nerve in rats. Methods 60 clean grade healthy male SD rats were divided into 3 groups randomly： normal group with 12 rats （24 eyes）, saline treatment group （control group） and valproate treatment group （treatment group） with 24 rats （24 eyes） in each group. No treatment was performed in normal group and the right optic nerve injury models were established by using nerve crush method in two experimental groups. The 300 mg/kg Sodium valproate was injected intraperitoneally in the treatment group, and the same volume of balance normal saline was injected intraperitoneally in control group respectively. The eyeball was enucleated at 3,7,14 and 21 days after injury, and the retinal slice were prepared. The pathological changes of retinal ganglion cell （RGC） were observed under light microscope, the expression of brain derived neurotrophic factor （BDNF） was studied through immunohistochemistry, and the average optical density （AOD） value of BDNF was tested by computer image analysis. Results Compared with the control group, the edema and vacuolization degree of ganglion cell layer ceils were lighter. The nucleus of RGC were arranged neatly in treatment group after Sodium valproate injection. At the same time, the AOD value and positive cell count of BDNF in treatment group was higher than control and normal group. Conclusion Sodium valproate can promote the BDNF expression after optic nerve injury, reduce RGC damage and has a protective effect on injured optic nerve.