Abstract Advanced glycosylation end products (AGEs) are harmful factors that can damage the inner blood–retinal barrier (iBRB). Rat retinal microvascular endothelial cells (RMECs) were isolated and cultured, and identified by anti-CD31 and von Willebrand factor polyclonal antibodies. Similarly, rat retinal Müller glial cells (RMGCs) were identified by H&E staining and with antibodies of glial fibrillary acidic protein and glutamine synthetase. The transepithelial electrical resistance (TEER) value was measured with a Millicell electrical resistance system to observe the leakage of the barrier. Transwell cell plates for co-culturing RMECs with RMGCs were used to construct an iBRB model, which was then tested with the addition of AGEs at final concentrations of 50 and 100 mg/L for 24, 48, and 72 h. AGEs in the in vitro iBRB model constructed by RMEC and RMGC co-culture led to the imbalance of the vascular endothelial growth factor (VEGF) and pigment epithelial derivative factor (PEDF), and the permeability of the RMEC layer increased because the TEER decreased in a dose- and time-dependent manner. AGEs increased VEGF but lowered PEDF in a dose- and time-dependent manner. The intervention with AGEs led to the change of the transendothelial resistance of the RMEC layer likely caused by the increased ratio of VEGF/PEDF.

中文翻译：

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体外共培养细胞模型中高级糖基化终产物对内血-视网膜屏障的影响

摘要 高级糖基化终产物 (AGEs) 是可破坏内部血-视网膜屏障 (iBRB) 的有害因素。分离培养大鼠视网膜微血管内皮细胞（RMECs），通过抗CD31和von Willebrand因子多克隆抗体鉴定。类似地，通过 H&E 染色和胶质纤维酸性蛋白和谷氨酰胺合成酶的抗体鉴定了大鼠视网膜 Müller 神经胶质细胞 (RMGC)。使用 Millicell 电阻系统测量跨上皮电阻 (TEER) 值以观察屏障的泄漏。使用用于共培养 RMGC 和 RMGC 的 Transwell 细胞板构建 iBRB 模型，然后通过添加终浓度为 50 和 100 mg/L 的 AGE 进行 24、48 和 72 小时的测试。RMEC与RMGC共培养构建的体外iBRB模型中AGEs导致血管内皮生长因子（VEGF）和色素上皮衍生因子（PEDF）失衡，由于TEER降低，RMEC层通透性增加。剂量和时间依赖性方式。AGEs以剂量和时间依赖性方式增加VEGF但降低PEDF。AGEs的干预导致RMEC层跨内皮电阻的变化，这可能是由VEGF/PEDF比值增加引起的。