Published online Dec 15, 2018. doi: 10.4239/wjd.v9.i12.239
Peer-review started: June 26, 2018
First decision: July 19, 2018
Revised: September 1, 2018
Accepted: November 2, 2018
Article in press: November 3, 2018
Published online: December 15, 2018
Diabetic retinopathy (DR) is a disease commonly associated with diabetes complications. It is known as one of the primary causes of visual impairment and blindness globally. More recent discoveries have shown that indicators of inflammation, altered vascular permeability, and increased production of inflammatory mediators occurs in the retina after 1-6 mo of the presence of diabetes. However, most of therapeutic approaches being developed do not address the early and potentially reversible failure of retinal perfusion.
Better understanding of the temporal sequence and stages of pathological disturbances of DR development is of scientific value, as it might contribute to improvements to current methods or even the development of new methods of diagnosis and treatment of the early and potentially reversible failure of retinal perfusion.
We have investigated the temporal sequence of pathological changes in the cellular structures of retina and choroidea in a rat model of alloxan-induced diabetes in the early stages of disease.
Alloxan accumulates in pancreatic cells, resulting in selective β-cell necrosis and diabetes. Experimental diabetes was modeled by three intraperitoneal injections (10 mg/100 g of weight) of an alloxan solution dissolved in physiological saline at 1-d intervals (total dose of alloxan 30 mg/100 g). The 30th and 60th days from the final alloxan injection were chosen as the endpoints of the experiment. Biochemical and enzyme immunoassay were performed. Furthermore, histological, immunohistochemical, and electron microscopy methods were employed to evaluate the rat’s eye slices. Similarly, light microscopy and morphometric analyses of slides were also conducted.
In the present study, the alloxan-induced diabetes model demonstrated that in the early stages of the disease, diabetic alterations in the structures of the retina and choroid are present, and these alterations progress with time. In the retina, DR manifest itself as a partial destruction of the structural-functional elements, namely, photoreceptors and are accompanied by a stromal reaction in the form of the development of interstitial edema and a reduction in the thickness of the retina due to photoreceptor destruction. The reduction in the number of blood vessels of the choroid, melanocytes, and pigment cells along with an increase in the number of macrophages were also observed at early stages of the disease.
The results of this study provide evidence that DR manifests itself at the early stages of diabetes. The starting point in the development of DR involves the early reduction in the number of melanocytes of the choroidea and the destruction of the retinal pigment epithelium, which are the primary components of the hematoretinal barrier.
Further studies that estimated vascular endothelial growth factor, prostate-derived Ets transcription factor, cytokines, NO, and antioxidants and correlated them with blood glucose levels and changes in the retina in various experimental models and at different time periods will contribute to the improvements and the development of new methods of diagnosis and treatment of DR.