Exploring the impact of oxidative stress, excitotoxicity, and apoptosis of retinal ganglion cells in streptozotocin-induced rats: A comprehensive investigation

Chronic hyperglycemia activates pathological molecular pathways, causing high inflammatory mediators, oxidative stress, and growth factors. This process contributes to retinal ganglion cell (RGC) apoptosis through the expression of N-methyl-D-aspartate (NMDA) receptors and nitric oxide (NO). This study analyzes the differential effect of NMDA receptor, NO expression, and RGC apoptosis in a hyperglycemic Wistar rat model. This research was designed as an experimental study, using a posttest only control group method. Fourteen male Wistar rats were split into two groups of seven: One received a single intraperitoneal injection of 50 mg/kg Streptozotocin (STZ) for hyperglycemia and the other served as the control. After 14 weeks of STZ injection, evaluations encompassed NMDA receptor, NO expression, and RGC apoptosis. Statistical analysis was performed using a parametric independent t -test and statistical significance was established at P < 0.05. The hyperglycemic group showed much higher NMDA receptor levels (11.77 ± 3.36) than the control group (4.21 ± 2.16), with a P < 0.001. The mean NO expression was 19.76 ± 8.41 in the hyperglycemic group, notably above the control group’s level of 4.01 ± 1.70 ( P < 0.001). The mean RGC apoptosis was 12.57 ± 3.26 in the hyperglycemic group and 9.00 ± 3.37 in the control group, without a significant difference, as indicated by a P = 0.068. These findings underscore the pronounced impact of hyperglycemia on NMDA receptors, NO expression, and RGC apoptosis, emphasizing potential targets for therapeutic interventions in diabetic retinopathy.