Anti-RAGE (Receptor Advanced Glycation End products) Antibody Improves Diabetic Retinopathy in Rats via Hypoglycemic and Anti-inflammatory Mechanism

Background: Receptor advanced glycation end products (RAGE) activation plays an essential role in diabetic retinopathy (DR) progression. This study was aimed to explore the role of anti-RAGE antibodies (RAGE antagonists) in inhibiting DR progression through their hypoglycemic and anti inflammatory mechanism in diabetic retinopathy induced rats.   Methods: A total of 30 male Wistar rats were randomly divided into five group. The group was consisted of normal control group, DR group without treatment, DR group with anti-RAGE 1 g/kg BW, 10 g/kg BW, and 100 g/kg BW. To assess the diabetic retinopathy, fundus photographs were taken every week using a camera with 16x magnification placed in front of the rat’s eyes. Blood glucose was checked by the glucose oxidase-peroxidase method. Retinal TNF- levels and VEGF were examined using an enzyme-linked immunosorbent assay (ELISA) kit.   Results: The finding of this study showed that anti-RAGE treatment at dose of 10 and 100 g/kg BW, HbA1c levels were significantly higher (p 0.05) compared to the normal control group but significantly lower (p 0.05) than in the diabetes group. The mean blood vessel diameter in the DR+anti-RAGE 10 and 100 g/kg BW groups was significantly lower than in the diabetic retinopathy group (p 0.05). The administration of anti-RAGE 10 and 100 g/kg BW showed the ability to significantly reduce VEGF levels compared to the DR group (p 0.05).   Conclusions:This study revealed at doses of 10 and 100 g/kg BW, anti-RAGE antibodies improved diabetic retinopathy in Wistar rats through hypoglycemic effects and anti-inflammatory mechanisms.