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目的检验氧化损伤的牛ＲＰＥ细胞是否存在着凋亡以及人参皂甙Ｒｇ１、Ｒｂ１和维生素Ｅ对其的影响，以期进一步研究ＲＰＥ细胞氧化损害的机理，并试图为预防和治疗与ＲＰＥ细胞相关的视网膜疾病提供有效的手段。方法建立牛ＲＰＥ细胞氧化损伤模型，利用原位末端标记技术测定ＲＰＥ细胞凋亡。结果发生凋亡的ＲＰＥ细胞细胞核染成紫蓝色，形态不一，往往成颗粒状着色，与次黄嘌呤（ＨＸ）／黄嘌呤氧化酶（ＸＯ）（ＨＸ＝０．１ｍｍｏｌ·Ｌ－１，ＸＯ＝５Ｕ·Ｌ－１）组阳性细胞数相比较，正常对照组Ｒｇ１（０．１ｍｇ·Ｌ－１）组及维生素Ｅ（１０ｍｇ·Ｌ－１）组存在显著性差异（Ｐ＜０．０５），而与Ｒｂ１（１０ｍｇ·Ｌ－１）组无显著性差异。结论氧化损伤可使培养的牛ＲＰＥ细胞发生凋亡。人参皂甙Ｒｇ１和维生素Ｅ对抗氧自由基对ＲＰＥ细胞损伤的机制可能是通过清除氧自由基、减少ＲＰＥ细胞脂类过氧化的发生，从而有效地抑制ＲＰＥ细胞凋亡，利于ＲＰＥ细胞的生存。
OBJECTIVE: To investigate the apoptosis of RPE cells oxidized by oxidative stress and the effects of ginsenoside Rg1, Rb1 and vitamin E on the oxidative damage of RPE cells in order to further study the mechanism of oxidative damage in RPE cells and to try to prevent and treat RPE cell-related retinal diseases Provide effective means. Methods The model of oxidative damage in RPE cells was established and the apoptosis of RPE cells was detected by in situ end labeling. Results The nuclei of apoptotic RPE cells were stained purple-violet in color and often colored in granular form. Compared with HX / xanthine oxidase (XO) (HX = 0.1 mmol·L-1, XO = 5U · L-1), there were significant differences between the groups of Rg1 (0.1 mg · L-1) and vitamin E (10 mg · L-1) ), But no significant difference with Rb1 (10mg · L-1) group. Conclusion Oxidative damage can induce the apoptosis of cultured bovine RPE cells. The mechanism by which ginsenoside Rg1 and vitamin E antagonize RPE cells may be due to the scavenging of oxygen free radicals and the reduction of lipid peroxidation in RPE cells, thus effectively inhibiting the apoptosis of RPE cells and promoting the survival of RPE cells.