目的：通过观察大鼠视网膜组织形态改变、细胞早期凋亡率、caspase-3和p53的表达，探讨细胞凋亡在模拟高海拔缺氧条件下大鼠视网膜损伤机制的作用。

方法：实验大鼠随机分为对照组和实验组。对照组为10只，饲养于海拔高度为1 500m的室内环境； 实验组为60只，分为6组，每组10只，分别饲养于模拟的海拔高度为5 000m的高原环境模拟实验舱中2、6、12、24、48、72h。各组大鼠处死后，每组分别采用苏木精-伊红染色观察大鼠视网膜病理形态的改变、免疫组化染色观察大鼠视网膜caspase-3和p53表达及流式细胞仪检测细胞早期凋亡率。

结果：模拟的高海拔缺氧条件可造成大鼠视网膜的组织损伤，且缺氧时间越长视网膜病理损伤越明显。caspase-3和p53的表达于2h检测到，随着缺氧时间增加，两者表达逐渐增加，差异具有统计学意义(P<0.05)。视网膜细胞早期凋亡率随缺氧时间逐渐上升，48h升高明显。

结论：细胞凋亡可能参与模拟高海拔缺氧的大鼠视网膜损伤机制，并通过caspase-3依赖的凋亡通路发挥作用。

AIM: To observe morphological changes of retinal tissues, early apoptosis rates and expressions of caspase-3 and p53 in rats, so as to analyze the mechanism of apoptosis in retinal damage of rats under stimulated hypoxic conditions at high altitude.

METHODS: Experimental rats were randomly divided into the control and experimental groups. Ten rats in the control group were bred in an indoor environment with the altitude of 1,500 meters; 60 in the experimental group were divided into 6 groups with each group of 10 rats, which were bred in a simulated experimental cabin of a simulated plateau environment with the altitude of 5,000 meters for 2, 6, 12, 24, 48 and 72h, respectively. After rats were killed in all groups, pathomorphological changes of rats' retinas were observed with hematoxylin eosin staining, expressions of caspase-3 and p53 in rats' retinas were noticed with immunohistochemical staining, and flow cytometry was used to detect early apoptosis rates.

RESULTS: The simulated hypoxic conditions at high altitude could cause rats' retinal tissues damage, and the longer hypoxic conditions were, the more obvious retinal pathological damage was. Expressions of caspase-3 and p53 were detected at 2h, and gradually increased with oxygen lack time increasing, the differences showed statistical significance(P<0.05). Early apoptosis rates of retinal cells gradually rose with oxygen lack time, and rose obviously at 48h.

CONCLUSION: Apoptosis may involve in the mechanism of rats' retinal damage induced by stimulated hypoxic conditions at high altitude, and play this role by the caspase-3-dependent apoptotic pathway.