Abstract

Objective: To investigate the effect of intravitreal injection of neural stem cells (NSC) induced from human umbilical cord mesenchymal stem cells, and to provide a theoretical basis for the clinical treatment of blood-retinal barrier damage due to diabetic retinopathy (DR). Methods: Experimental study. Sixty male Sprague-Dawley rats were randomly divided into control group, DR group and NSC group. Diabetic rats were induced by injection of streptozotocin, and the control rats were injected with an equal volume of solvent. Three months after the establishment of diabetic models, the NSC group was injected with 2 μl of NSC in the right vitreous, and the DR group was injected with 2 μl of phosphate-buffered saline. One month later, all the rats were sacrificed. The retinal vessels and leakage were examined with flat-mounted retinas. Vascular permeability was quantified by analyzing albumin leakage using the Evans blue (EB) method. Retina was examined by hematoxylin and eosin staining. Results: Retinal blood vessels of the control rats were normal, with no EB leakage outside the vessels. The background fluorescence was enhanced and focal leakage and focal dilated vessels were detected in the DR group. In the NSC group, background fluorescence was enhanced slightly and EB leakage area decreased significantly compared with the DR group. The average EB in control group, DR group and NSC group were (9.91±1.53), (24.67±2.26) and (12.85±2.58)μg/g, The EB leakage in the NSC group decreased significantly compared with the DR group (q=9.748, P<0.05). Pathological hematoxylin and eosin staining showed that the retinal layer structure was normal and clear in the control group, the retina was thin, the cell arrangement was in disorder and the nucleus was swelling in the DR group, the status of the NSC group was between the other two groups. Conclusions: Transferring human umbilical cord mesenchymal stem cells-induced NSC in vitro to diabetic rat models by intravitreal injection could reduce leakage of blood vessels and attenuate blood-retinal barrier breakdown induced by diabetes. (Chin J Ophthalmol, 2017, 53: 53-58).

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