方法：选取健康雌性SD大鼠60只随机分为：空白组、模型组和实验组，每组各20只。采用视神经夹伤方法，建立大鼠视神经急性损伤模型。模型组制作视神经损伤模型成功后即刻向玻璃体腔注射平衡盐溶液5μL，之后的1、2wk分别向玻璃体腔注射平衡盐溶液5μL； 而实验组在视神经损伤模型制作成功后即刻向玻璃体腔注射PEDF 5μL，同样在1、2wk时分别向玻璃体腔注射PEDF 5μL。通过HE 染色，光镜下观察视网膜形态学变化并且对视网膜神经节细胞进行计数。通过免疫组织化学半定量的方法对Bcl-2和Bax的表达进行检测，观察PEDF对受损视神经的影响。

结果：HE染色观察，实验组神经节细胞从细胞形态上要好于模型组，且RGCs数量较模型组多。实验组的Bcl-2和Bax的蛋白表达与空白组、模型组比较，差异有统计学意义(P<0.05)，实验组较模型组Bcl-2蛋白表达增加，Bax蛋白表达下降。

结论：PEDF可通过上调视网膜Bcl-2蛋白的表达、减弱Bax蛋白表达，以减弱或抑制视神经损伤后RGCs的细胞凋亡，减轻视神经损伤。

METHODS: Totally 60 healthy female SD rats were randomly divided into three groups: blank group, model group and experimental group, 20 rats in each group. Acute injury model of optic nerve in rats are established by crushing optic nerve. After the model of optic nerve injury was made successfully in model group, the rats were injected with balanced salt solution 5μL into vitreous cavity, and at 1 and 2wk later respectively they were injected again. In experimental group, after the model of optic nerve injury was made successfully, immediately the rats were injected with the PEDF 5μL into vitreous cavity, also at 1 and 2wk later respectively they were injected again. To observe the retinal morphologic changes and count the number of retinal ganglion cells, the specimen was given HE staining and observed under light microscope. The immunohistochemical semi quantitative method was used to detect the expression of Bcl-2 and Bax to observe the effect of PEDF on the optic nerve after injury.

RESULTS: Cell morphology of ganglion cells in experimental group was better and the number of RGCs was much more, comparing with the model group by HE staining. The expression of Bcl-2 and Bax in the experimental group was significantly different with that in the blank group and the model group(P<0.05). The expression of Bcl-2 increased and the expression of Bax decreases in the experimental group compared with the model group.

CONCLUSION: PEDF can inhibit or weak the apoptosis of RGCs cells after optic nerve injury and alleviate the injury of optic nerve by increasing the expression of Bcl-2 protein or decreasing the expression of Bax protein.