目的：探讨大鼠视网膜缺血再灌注损伤(retinal ischemia-reperfusion injury,RIRI)过程中黄芪对Bcl-2和Bax蛋白表达的影响及作用机制。 方法：前房加压法制作实验性RIRI的大鼠模型。将66只SD大鼠随机分为正常组、缺血再灌注模型组、黄芪注射液治疗组。后两组各分为 6，12，24，48h和3d五个时间段，HE染色后光镜下观察视网膜组织变化, 采用免疫组织化学法与Western-blot法测定大鼠RIRI后视网膜中Bcl-2和Bax蛋白表达的变化。 结果：Bcl-2和Bax在正常视网膜组织中几乎不表达，在缺血再灌注6h开始表达，24h表达显著，48h开始下降，3d后表达已经明显减弱。黄芪注射液治疗组各观察指标变化趋势基本与单纯缺血再灌注组相似。黄芪注射液治疗组与模型组比较,Bcl-2表达均明显增强,Bax表达均明显减弱，两组间比较差异均有显著统计学意义(P<0.01)。 结论：黄芪注射液预处理可使神经节细胞Bcl-2表达增强，Bax表达减弱，减少神经节细胞凋亡，对RIRI神经节细胞有明显的保护作用。

AIM:To investigate the expression and mechanism of Bcl-2 and Bax protein in retinal ischemia-reperfusion injury(RIRI) in rats, as well as the effect of Astragalus (AS) on it. METHODS: The models of RIRI were made by transient elevating of intraocular pressure. A total of 66 SD rats were randomly divided into normal control group, ischemia-reperfusion model group and AS treatment group. The last two groups were subdivided into 6, 12, 24, 48 hours, and 3 days small groups according to the different reperfusion time. The light microscope was used to observe the structural changes in retina. Western-blot and immunohistochemitry were used to measure changes of Bcl-2 and Bax protein levels in retinal tissue.  RESULTS:No expression of Bcl-2 and Bax positive cells were found in normal group.At the ischemia-reperfusion groups,the expression of Bcl-2 and Bax began to increase at 6 hours after reperfusion．At 24 hours after reperfusion the expression reached the peak, and went on increasing with the reperfusion time prolonged，and began to decrease after 3 days. The therapy groups of Astragalus had the same trend with the ischemic groups in each index.Astragalus injection treatment group being compared with model group, Bcl-2 expression was significantly stronger and Bax expression was significantly reduced. There was significant difference between two groups(P<0.01). CONCLUSION: Astragalus injection pretreatment allows Bcl-2 expression of ganglion cells enhanced and expression of Bax diminished, and reduces ganglion cells apoptosis,which have a significant protective effect on the RIRI ganglion cells.