Danilova Irina, Medvedeva Svetlana, Shmakova Svetlana, Chereshneva Margarita, Sarapultsev Alexey, Sarapultsev Petr
Department of Biology and Fundamental Medicine, Institute of Natural Sciences and Mathematics, Ural Federal University Named After the First Pres. of Russia B.N. Yeltsin, Ekaterinburg 620002, Russia.
Laboratory of Immunophysiology and Immunopharmacology, Institute of Immunology and Physiology, Ural Division of Russian Academy of Sciences, Ekaterinburg 620049, Russia.
World J Diabetes. 2018 Dec 15;9(12):239-251. doi: 10.4239/wjd.v9.i12.239.
To investigate the temporal sequence of pathological changes in the cellular structures of retina and choroidea in the early stages of diabetes in laboratory animals.
Experimental type 1 diabetes was modeled by three intraperitoneal injections of an alloxan solution into 30 male nonlinear rats at 16 wk of age. The 30 and 60 days from the final alloxan injection were chosen as the endpoints. Light and electron microscopy and morphometric and immunohistochemical studies were performed on histological slices of eyeballs from experimental animals.
Diabetic disturbances progressed to 60 d of the experiment. Thus, in the retina, a partial destruction of photoreceptors accompanied by interstitial edema was observed. The morphometric analysis revealed a reduction in the thickness of the retina. A reduction in the number of blood vessels of the choroid with disturbances of the endothelial cells and the vascular walls and a persistent reduction in the number of melanocytes were observed. The number of proliferating Ki-67 positive cells decreased, and the number of macrophages increased with diabetes development.
The starting point in the development of destructive changes involves early reduction in the number of melanocytes of the choroidea and alterations in the retinal pigment epithelium.
研究实验动物糖尿病早期视网膜和脉络膜细胞结构病理变化的时间顺序。
对30只16周龄雄性非肥胖大鼠腹腔注射三次四氧嘧啶溶液,建立实验性1型糖尿病模型。选取末次注射四氧嘧啶后30天和60天作为观察终点。对实验动物眼球组织切片进行光镜和电镜检查以及形态计量学和免疫组织化学研究。
糖尿病病变持续至实验第60天。在视网膜中,观察到光感受器部分破坏并伴有间质水肿。形态计量学分析显示视网膜厚度减小。脉络膜血管数量减少,内皮细胞和血管壁出现病变,黑素细胞数量持续减少。随着糖尿病发展,增殖的Ki-67阳性细胞数量减少,巨噬细胞数量增加。
破坏性变化发展的起始点涉及脉络膜黑素细胞数量早期减少以及视网膜色素上皮改变。