Aleman-Flores Rafael, Mompeo-Corredera Blanca
Department of Morphology, University of Las Palmas de Gran Canaria, Spain.
J Ophthalmic Vis Res. 2018 Oct-Dec;13(4):433-438. doi: 10.4103/jovr.jovr_130_17.
This study analyzes the structures of optic nerve elements, i.e., glial cells and nerve fibers, in an STZ-induced hyperglycemic animal model. Morphological changes in glial elements of the optic nerve in hyperglycemic and normoglycemic animals were compared.
Transmission electron microscopy, histochemistry, immunohistochemistry, and morphometry were used in this study.
Hyperglycemia increased the numbers of inner mesaxons and axons with degenerative profiles. Furthermore, it led to both an increase in the amount of debris and in the numbers of secondary lysosomic vesicles in glial cytoplasm. Hyperglycemia also led to a decrease in glial fibrillary acidic protein expression and an increase in periodic acid-Schiff-positive deposits in the optic nerves of hyperglycemic animals.
We conclude that the damage to the structural elements observed in our animal models contributes to the pathogenesis of optic neuropathy in the early stages of diabetes.
本研究分析链脲佐菌素诱导的高血糖动物模型中视神经元件(即神经胶质细胞和神经纤维)的结构。比较了高血糖和正常血糖动物视神经胶质元件的形态学变化。
本研究采用透射电子显微镜、组织化学、免疫组织化学和形态测量法。
高血糖增加了内中轴突和具有退行性特征的轴突数量。此外,它导致神经胶质细胞质中碎片数量和次级溶酶体囊泡数量均增加。高血糖还导致高血糖动物视神经中胶质纤维酸性蛋白表达减少,过碘酸希夫氏阳性沉积物增加。
我们得出结论,在我们的动物模型中观察到的结构元件损伤有助于糖尿病早期视神经病变的发病机制。