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Academic Journal of Second Military Medical University ; (12): 977-983, 2019.
Article in Chinese | WPRIM | ID: wpr-838038

ABSTRACT

Objective: To establish streptozotocin (STZ)-induced diabetic retinopathy model in mice, and to observe the pathological changes of the retina in early diabetic stages and the expression of vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor (VEGFR)1 and VEGFR2 in the mouse model. Methods: C57BL/6J mice, aged 6-8 weeks, received intraperitoneal injection of STZ (55 mg/kg) once a day for 5 d. The fasting blood glucose concentration was measured 1 week after injection. The diabetic and control mice were fed for 5 months. Then the morphological changes of retina in diabetic mice were analyzed by H-E staining, Evans blue perfusion angiography and retinal vascular network digestion. The expression of VEGF and its receptors VEGFR1, VEGFR2 in diabetic retinopathy was analyzed by quantitative real-time PCR and Western blotting. Results: Compared with the control group, the blood glucose levels of the model group were significanlty increased 1 week, 1 to 5 months after injection (all higher than 16.5 mmol/L, all P<0.01). At 5 months after injection, the whole retina of the model group became thinner; the number of photoreceptor cells, inner and outer nuclear cells were decreased and disorderly arranged; the blood vessels went tortuously with leakage and leakage spots; the number of vascular endothelial cells was increased, with altered morphology; the number of peripheral cells was decreased; and there were no cellular capillaries and lumen occlusion. The expression levels of VEGF, VEGFR1 and VEGFR2 protein and mRNA were significantly increased in the model group compared with the control group (all P < 0.01). Conclusion: Diabetic retinopathy mouse model has been successfully constructed, with proliferative diabetic retinopathy appearing 5 months after diabetes, and the expression levels of VEGF, VEGFR1 and VEGFR2 are increased in the retina of diabetic mice.

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