Abstract
Objective The purpose of this project is to make sequential and indepth observation of the variations of retinal microvascular, microstructure, and inflammatory mediators at the early stage of diabetic retinopathy (DR) in streptozotocin-induced diabetes mellitus (DM) rats. Methods DM was induced by a single intraperitoneal injection of 60 mg/kg body weight streptozotocin (STZ). The fluorescein fundus angiography, hematoxylin and eosin staining, periodic acid-Schiff staining, fluorescence imaging techniques, quantitative real-time PCR, and vascular endothelial growth factor- (VEGF-) A ELISA were performed on the 8th day, at the 4th week, 6th week, 8th week, and 10th week after DM induction, respectively. Results In this study, we observed not only the decrease of retinal ganglion cells (RGCs) and the increase of endotheliocytes to pericytes (E/P) ratio, acellular capillaries, and type IV collagen-positive strands began to occur on the 8th day after induction but the vascular permeability and new vessel buds began to appear in the diabetes group at the 8th week, while the expression of VEGF-A, VEGF mRNA, IL-6 mRNA, ICAM mRNA, and TNF-α mRNA were significantly higher in the diabetes group compared with the normal group(P < 0.01) on the 8th day after induction and maintained a high expression level throughout the 10-week observation period. However, the expression of CD18 mRNA began to increase significantly at the 4th week after induction and reached a peak at the 6th week. Conclusion Our study indicated the abnormal alterations of microvessels, microstructure, and inflammatory mediators at the early stage of DR, which confirms and supplements the previous research, and also promotes an indepth understanding and exploration of the pathophysiology and underlying pathogenesis of DR.
Highlights
Diabetic retinopathy (DR) remains a leading cause of vision loss in the working age population of industrialized regions [1]
A variety of inflammatory mediators on the retina can be upregulated in the early stage of diabetes, including intercellular adhesion molecule-1 (ICAM-1), vascular endothelial growth factor (VEGF), nuclear factor kappa B (NF-κB), inducible nitric oxide synthase, tumor necrosis factor (TNF)-α, CD18, and local inflammatory response playing an important role in the occurrence and development of DR [4, 5]
It has become increasingly clear that diabetic retinopathy affects retinal vasculature and retinal neuronal and glial cells and a variety of inflammatory mediators [4, 5, 13,14,15,16,17] (Figure 9)
Summary
Diabetic retinopathy (DR) remains a leading cause of vision loss in the working age population of industrialized regions [1]. Due to the fact that the patients without typically asymptomatic, NPDR (especially the mild NPDR) usually represents the early stage of DR. Diabetic retinopathy is mainly characterized by loss of pericytes and retinal ganglion cells (RGCs), overexpression of vascular endothelial growth factor (VEGF), and compensatory synthesis and deposition of extracellular proteins. A variety of inflammatory mediators on the retina can be upregulated in the early stage of diabetes, including intercellular adhesion molecule-1 (ICAM-1), VEGF, nuclear factor kappa B (NF-κB), inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)-α, CD18, and local inflammatory response playing an important role in the occurrence and development of DR [4, 5]
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