Cell Therapy Center, Xuanwu Hospital, Capital Medical University, Beijing, China.
Cornea. 2012 Dec;31(12):1455-9. doi: 10.1097/ICO.0b013e3182490907.
The purpose of this study was to investigate the ultrastructural corneal changes of chronic diabetic monkeys and explore the relationship between advanced glycation end products and ultrastructural changes in diabetic corneas.
A total of 8 cynomolgus monkeys were used in this experiment. Four monkeys were induced into insulin-dependent diabetes mellitus for 4 years. Four age-matched healthy monkeys were used as the controls. Ultrathin sections obtained from the corneas were examined by transmission electron microscopy.
Advanced glycation end product immunoreactivity was observed in the epithelial cells, epithelial basement membrane, and stromal keratocytes of diabetic corneas, whereas advanced glycation end product immunoreactivity was not found in the corresponding area in normal corneas. Abnormal collagen fibril bundles of variable thickness were identified in corneal stroma in all diabetic monkeys. Epithelial and endothelial cell degeneration was also observed in 1 diabetic monkey.
Abnormal aggregates of collagen fibrils in stromal matrix were common among long-term diabetic monkeys, and the formation of the abnormal collagen fibril aggregates might result from excessive nonenzymatic glycosylation.
本研究旨在观察慢性糖尿病猴角膜的超微结构变化，探讨糖基化终产物与糖尿病角膜超微结构变化的关系。
本实验共使用 8 只食蟹猴。4 只猴子被诱导成胰岛素依赖性糖尿病 4 年。4 只年龄匹配的健康猴子作为对照。用透射电镜观察角膜超薄切片。
糖尿病猴角膜上皮细胞、上皮基底膜和基质角膜细胞中可见糖基化终产物免疫反应性，而正常角膜相应区域未见糖基化终产物免疫反应性。所有糖尿病猴的角膜基质中均发现胶原纤维束异常，厚度不一。在 1 只糖尿病猴中还观察到上皮细胞和内皮细胞变性。
长期糖尿病猴的基质中胶原纤维束异常聚集较为常见，异常胶原纤维束的形成可能是由于非酶糖基化过度所致。
