Document Type : Original Article

Authors

1 Ph.D. candidate, Department of Biochemistry, Medical School, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

2 Department of Ophthalmology, Infectious Ophthalmic Research Center, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

3 Department of Biochemistry, Medical School, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

4 Associate Professor, Department of Biochemistry, Cellular & Molecular Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

Abstract

Background: There is a direct correlation between ocular vascular endothelial growth factor (VEGF) level and progression of pathological outcomes in diabetic retinopathy. In our previous study, the periocular administration of propranolol and celecoxib could significantly reduce ocular VEGF levels in a diabetic mouse model. Here, we investigated the changes of serum VEGF after periocular administration of propranolol and celecoxib in a diabetic mouse model.
Methods: Forty male BALB-C mice aged 4-6 weeks were divided into four groups as follows: non-diabetic, streptozotocin-induced diabetic, streptozotocin-induced diabetic + periocular injection of 200 µg celecoxib and streptozotocin-induced diabetic + periocular injection of 10 µg propranolol. Serum VEGF in all experimental groups was measured by using enzyme-linked immunosorbent assay (ELISA) method.
Results: In comparison to the non-diabetic group, serum VEGF levels were markedly elevated in diabetic groups and periocular injection of anti-VEGF agents could affect serum VEGF levels. Celecoxib was significantly more effective than propranolol in regulating serum VEGF levels.
Conclusion: The periocular injection of both celecoxib and propranolol is one of the most effective ways to prevent diabetic retinopathy and also has a beneficiary effect on down-regulation of serum VEGF levels in a diabetic mouse model. Therefore, periocular injection of anti-VEGF agents can play a significant role in preventing clinical side effects of diabetes.

Keywords

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