银杏叶提取物对大鼠视神经夹伤后视网膜神经节细胞的保护作用

The protective effect of Ginkgo biloba extract on retinal ganglion cells after optic nerve crush in rats

目的研究银杏叶提取物EGb761对大鼠视神经夹伤后视网膜神经节细胞凋亡的保护作用。方法将40只Wistar大鼠随机分为实验组和对照组，每组20只，每只大鼠均建立实验性右眼视神经钳夹伤模型，伤后1h，实验组球后注射银杏叶提取物EGb7610．05ml（60mg／kg），对照组球后注射0．05ml平衡盐溶液，两组均隔日注射1次，直至处死。于损伤后3d．7d、14d取材，观察不同时间段视网膜形态学变化及视网膜神经节细胞凋亡情况。采用免疫组化技术检测各组Bcl-2及Bax的蛋白表达水平。结果光镜下实验组和对照组均可见视网膜神经节细胞凋亡。随病程延长凋亡的细胞逐渐增多，实验组凋亡细胞数目较对照组少，差异有统计学意义（P〈0．05）。实验组Bcl-2蛋白表达水平明显高于对照组，实验组Bax蛋白表达水平及Bax／Bcl-2比值则明显低于对照组差异均有统计学意义（P〈0．05）。结论银杏叶提取物能减少大鼠视神经夹伤后视网膜神经节细胞凋亡，对视网膜神经节细胞有明显的保护作用。其机制可能与凋亡相关基因Bcl-2，Bax蛋白表达水平变化有关。

Objective To study the protective effect of Ginkgo biloba extract EGb761 on retinal ganglion cells after optic nerve crush in rat. Methods Forty Wistar rats were divided into experimental and control groups at random. The optic nerves crushed model were made. After 1 h, EGb761 0.05 ml （60 mg/ kg ） was injected into the retrobulbar area of injury eyes in experimental group. Balanced salt solution 0.05 ml was injected in control group. The rats in the two groups received injection every other day. On the 3,7 and 14 d after injury, the eyeballs were enueleated for observing the changes of the retina and RGCs apoptosis. The expression of Bcl-2 and Bax protein were measured with immunohistochemical technique. Results The apoptosis of RGCs in experimental and control groups were seen under microscope. With the extension of injury course, positive ceils of apoptosis were increased gradually. The numbers of apoptosis ceils in the experimental group were lower than that in the control group, and there were statistically significant difference （P 〈 0.01 ）. The expression of bcl-2 protein in experimental group was significantly higher than that in the control group. The expression of Bax protein and the ratio of Bax/Bcl-2 in the experimental group were lower than that in the control group （ P 〈 0.05 ）. Conclusion Ginkgo biloba extract can reduce apoptosis of retinal ganglion cells after rats optic nerve crush, showing obvious protective effect on retinal ganglion cells. The mechanism may be related to the expression of apoptosis gene Bax and Bcl-2.