目的 分析长链非编码RNA母系表达基因3（LncRNA MEG3）通过调控视网膜环氧合酶-2/前列腺素E2/血管内皮生长因子（COX-2/PGE2/VEGF）信号通路对早期糖尿病大鼠视网膜的保护作用。 方法 选取SPF级50只SD大鼠，10只大鼠作为对照组，40只构建糖尿病视网膜病变模型，共有32只大鼠建模成功，分为模型组8只、阴性对照组8只、MEG3过表达组8只、MEG3过表达+COX-2抑制剂组8只。观察各组大鼠病理组织学、血管通透性、糖脂代谢、炎症因子、氧化应激指标、PGE2水平、COX-2/VEGF mRNA与蛋白相对表达量。 结果 与对照组相比，模型组HDL-C、CAT、GSH-PX、SOD降低，血管通透性、TG、TC、LDL-C、IL-6、IL-1β、TNF-α、MDA、PGE2、COX-2、VEGF mRNA、蛋白相对表达量升高（P < 0.05）；与阴性对照组相比，MEG3过表达组HDL-C、CAT、GSH-PX、SOD升高，血管通透性、TG、TC、LDL-C、IL-6、IL-1β、TNF-α、MDA、PGE2、COX-2、VEGF mRNA、蛋白相对表达量降低（P < 0.05）；与MEG3过表达组相比，MEG3过表达+ COX-2抑制剂组HDL-C、CAT、GSH-PX、SOD升高，血管通透性、TG、TC、LDL-C、IL-6、IL-1β、TNF-α、MDA、PGE2、COX-2、VEGF mRNA、蛋白相对表达量降低（P < 0.05）。 结论 LncRNA MEG3可通过调节COX-2/PGE2/VEGF通路，改善大鼠糖脂代谢水平，抑制炎症因子表达，降低应激反应，减轻糖尿病视网膜病变。

Objective To investigate the protective effect of LncRNA MEG3 on the retina in early-stage diabetic rats through regulation of the COX-2/PGE2/VEGF signaling pathway. Methods 50 male SD rats of SPF grade were selected for the study. Among them， 10 rats were assigned to the control group， while 40 rats were used to establish diabetic retinopathy models. A total of 32 rats successfully underwent modeling and were subsequently divided into four groups （n = 8 per group）： model group， negative control group， MEG3 overexpression group， and MEG3 overexpression + COX-2 inhibitor group. Histopathological changes， vascular permeability， glucose and lipid metabolism， inflammatory factors， oxidative stress indices， PGE2 levels， as well as the relative mRNA and protein expression levels of COX-2 and VEGF were evaluated in each group. Results Compared with the control group， HDL-C， CAT， GSH-PX， and SOD levels were significantly decreased， whereas the mRNA and protein expression levels of vascular permeability， TG， TC， LDL-C， IL-6， IL-1β， TNF-α， MDA， PGE2， COX-2， and VEGF were significantly increased in the model group （P < 0.05）. Compared with the negative control group， HDL-C， CAT， GSH-PX， and SOD levels were significantly increased in the MEG3 overexpression group， while the mRNA and protein expression levels of vascular permeability， TG， TC， LDL-C， IL-6， IL-1β， TNF-α， MDA， PGE2， COX-2， and VEGF were significantly decreased （P < 0.05）. Compared with the MEG3 overexpression group， HDL-C， CAT， GSH-PX， and SOD levels were further increased in the MEG3 overexpression + COX-2 inhibitor group， and the mRNA and protein expression levels of vascular permeability， TG， TC， LDL-C， IL-6， IL-1β， TNF-α， MDA， PGE2， COX-2， and VEGF were further decreased （P < 0.05）. Conclusion LncRNA MEG3 is capable of regulating the COX-2/PGE2/VEGF pathway， enhancing glucose and lipid metabolism in rats， suppressing the expression of inflammatory factors， attenuating stress responses， and alleviating diabetic retinopathy.