目的 探讨延龄草苷对高糖诱导的人视网膜血管内皮细胞（HRVEC）损伤的影响及作用 机制。方法 5、10、20 μmol/L 的延龄草苷作用于 30 mmol/L 葡萄糖诱导的 HRVEC 细胞，或 30 mmol/L 葡萄糖诱导转染 miR⁃1247⁃3p 模拟物的 HRVEC 细胞，或 20 μmol/L 的延龄草苷作用于 30 mmol/L 葡萄糖诱导的 转染 miR⁃1247⁃3p 抑制剂的 HRVEC 细胞，DCFH⁃DA 法检测细胞中 ROS 水平，酶联免疫吸附法检测 MDA 和 SOD 水平，流式细胞仪检测细胞凋亡，Western blot 法检测Bcl⁃2和Bax 蛋白表达，RT⁃qPCR 法检测miR⁃1247⁃ 3p 表达。结果 延龄草苷降低了高糖诱导的 HRVEC 中 ROS 和 MDA 水平、凋亡率及 Bax 蛋白表达（P < 0.05），提高了 SOD 活性、Bcl⁃2 蛋白表达及 miR⁃1247⁃3p 表达（P < 0.05），且呈剂量依赖性。过表达 miR⁃ 1247⁃3p 降低了高糖诱导的 HRVEC 中 ROS 和 MDA 水平、凋亡率和 Bax 蛋白表达（P < 0.05），提高了 SOD 活 性和 Bcl⁃2 蛋白表达（P < 0.05）。抑制 miR⁃1247⁃3p 逆转延龄草苷对高糖诱导的 HRVEC 细胞氧化应激和凋 亡的影响（P < 0.05）。结论 延龄草苷可能通过上调 miR⁃1247⁃3p 表达抑制高糖诱导的 HRVEC 细胞氧化应激和凋亡，减轻细胞损伤。

Objective To investigate the effect and mechanism of trillin on high glucose⁃induced retinal vascular endothelial cells（HRVEC）injury. Methods 5，10，and 20 μmol/L of trillin were applied to HRVEC cells induced by glucose of 30 mmol/L，or 30 mmol/L of glucose was induced HRVEC cells transfected with miR⁃ 1247⁃3p mimic，or 20 μmol/L of trillin was applied to 30 mmol/L glucose⁃induced HRVEC cells transfected with miR⁃1247⁃3p inhibitor. DCFH⁃DA method was used to detect intracellular ROS level；enzyme⁃linked immunosor⁃ bent assay was used to detect levels of MDA and SOD；flow cytometry was used to detect cell apoptosis；Western Blot method was used to detect the protein expression levels of Bcl⁃2 and Bax；RT⁃qPCR method was used to detect the expression level of miR⁃1247⁃3p. Results Trillin reduced the levels of ROS and MDA，apoptosis rate， and protein expression of Bax in glucose⁃induced HRVEC cells（P < 0.05），while increased SOD activity and expressions of Bcl⁃2 protein and miR⁃1247⁃3p（P < 0.05）in a dose⁃dependent pattern. Overexpression of miR⁃1247⁃ 3p reduced the levels of ROS and MDA，apoptosis rate，and protein expression of Bax in glucose⁃induced HRVEC cells（P < 0.05），while increased SOD activity and expression of Bcl⁃2 protein（P < 0.05）. Inhibition of miR⁃1247⁃ 3p reversed the effect of trillin on oxidative stress and apoptosis of HRVEC cells induced by high glucose（P < 0.05）. Conclusions Trillin may inhibit high glucose⁃induced oxidative stress and apoptosis in HRVEC cells by up⁃regu⁃ lating the expression of miR⁃1247⁃3p，alleviating cell damage.