Objective: Hyperglycemia-induced oxidative stress has been shown to induce retinal cell apoptosis. It also stimulates angiogenesis in retinal vasculature by increasing vascular endothelial growth factor (VEGF) expression. Retinal cell apoptosis and angiogenesis are the hallmark features of diabetic retinopathy. In this study, we investigated the role of tocotrienol-rich fraction (TRF), a potent antioxidant, towards reducing retinal cell apoptosis and retinal VEGF expression in rats with streptozotocin (STZ)-induced diabetic retinopathy. Methods: 200-250 g Sprague-Dawley rats were divided into three groups; control rats (N) which received intraperitoneal injection of citrate buffer, and diabetic control rats (DV) and diabetic TRF-treated rats (DT). The diabetes was induced with intraperitoneal injection of STZ (55 mg/kg body weight). After confirmation of the diabetic status, DT received 100 mg of TRF/kg body weight via oral gavage once daily for 12 weeks, whereas DV and N similarly received vehicle. After the completion of treatment period, rats were euthanized, eyeballs were enucleated and processed for terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) staining to detect apoptotic retinal cells. Additionally, retinas were collected for measurement of VEGF expression using ELISA. TUNEL-positive retinal cells were quantified in ganglion cell layer (GCL) region. Results: Higher TUNEL-positive retinal cell count in GCL was observed in DV and DT compared to N (p<0.001). However, DT showed significantly lesser number of TUNEL positive cells in GCL compared to DV (p<0.05). The retinal VEGF expression positively correlated with the extent of retinal cell apoptosis, whereby, significantly lower VEGF expression was detected in DT compared to DV (p<0.05). Conclusion: Oral treatment with TRF reduces retinal cells apoptosis and VEGF expression in rats with STZ-induced diabetic retinopathy.