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目的 :了解早期糖尿病角膜组织的超微变化 ,探讨糖尿病角膜病变的发病机制。方法 :选取SD雄性大鼠 4 0只 ,随机分为糖尿病组和正常对照组 ,前者以链脲佐菌素诱导成糖尿病模型。分别于 6、8、10、12周取角膜 ,扫描电镜及透射电镜下观察其超微改变。结果 :各个观察时点糖尿病大鼠角膜上皮和内皮细胞水肿 ,胞浆内线粒体增多和肿胀 ,随着病程进度而明显 ;角膜内皮的破坏从周边开始 ,逐渐向中央发展 ;成模后第 10周开始出现基质层胶原纤维排列紊乱 ,部分呈格子状排列 ,有断裂现象。结论 :糖尿病性角膜病变超微结构的改变导致了角膜功能异常 ,这可能与高血糖时物质代谢异常有关。
Objective: To understand the ultrastructural changes of early diabetic corneal tissue and to explore the pathogenesis of diabetic corneal disease. Methods: Forty SD male rats were randomly divided into diabetic group and normal control group. The former was induced by streptozotocin into diabetic model. The corneas were taken at 6, 8, 10, and 12 weeks respectively. The ultrastructural changes were observed under scanning electron microscope and transmission electron microscope. Results: The edema of corneal epithelium and endothelium, the increase of mitochondria and swelling in cytoplasm of diabetic rats were observed at different time points. The corneal endothelium destroyed gradually from the periphery to the central part of the cornea. The stromal collagen fibers began to disorder, part of the grid-like arrangement, a fracture phenomenon. CONCLUSION: Alteration of the ultrastructure of diabetic corneal lesions leads to corneal dysfunction, which may be related to the abnormal metabolism of blood glucose.