方法：人RPE细胞系传代培养，MTT检测细胞活力，流式细胞仪检测细胞凋亡率，透射电镜观察超微结构变化。

结果：MTT结果显示用10^-8mol/L和10^-4mol/L AST处理后，RPE细胞活性分别提高到53.66%±3.25%和70.43%±2.38%，与氧化损伤组(38.76%±3.74%)比较，差异具有统计学意义(P<0.05)； 流式细胞计数结果显示，预先给予10^-8mol/L和10^-4mol/L的AST作用后，RPE细胞凋亡率分别下降到30.23%±1.91%和12.58%±2.12%，与氧化损伤组(42.50%±1.94%)比较，差异具有统计学意义(P<0.05)。电镜观察结果显示，伴随AST作用浓度的增加，细胞形态亦逐渐得到改善。

结论：AST可以抑制H₂O₂诱导的人RPE细胞的凋亡，从而为寻求有效的防治视网膜损伤的药物提供可靠的实验依据。

METHODS:Human RPE cells were subcultured, cell activity was detected by MTT, rate of apoptosis was detected by flow cytometry and cell ultrastructure changes were observed under transmission electron microscope.

RESULTS:MTT results showed that cell activity elevated to(53.66%±3.25% and 70.43%±2.38% after 10^-8mol/L and 10^-4mol/L AST treated. The difference had statistically significant(P<0.05)compared with oxidative injury group(38.76%±3.74%). Flow cytometry results showed that the apoptosis rate of RPE cells decreased to 30.23%±1.91% and 12.58%±2.12% in AST pretreated group, the difference was significant(P<0.05)compared with oxidative injury group(42.50%±1.94%); Electron microscopy showed that the morphology of cells gradually improved accompanied with the concentration of AST elevated.

CONCLUSION:AST may inhibit hydrogen peroxide-induced apoptosis of RPE cells, it can provide reliable evidence for pursue effective medicine to prevent and treat retina injury.