We aimed to assess the effects of naringenin on oxidative damage and cell apoptosis in diabetic retinopathy rats via the nuclear factor erythroid 2-related factor 2/antioxidant response element signaling pathway. 70 rats were randomly divided into normal and model groups. Diabetic model was established through continuous intraperitoneal injection of streptozotocin. Model rats were further randomly divided into model, low dose and high dose groups. Body weight and blood glucose level changes were observed. Retinal thickness was detected through optical coherence tomography. The content of malondialdehyde, activities of superoxide dismutase and glutathione peroxidase and number of reactive oxygen species-positive cells in retinal tissues were determined. Cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. The protein expressions of nuclear factor erythroid 2-related factor 2, NAD(P)H quinone oxidoreductase 1 and heme oxygenase-1 were detected by western blotting. Compared with model group, body weight rose; while blood glucose level and retinal thickness declined in low and high dose groups. The number of reactive oxygen species-positive cells decreased in high dose group compared with that in model group. Malondialdehyde content and apoptotic index increased, while superoxide dismutase and glutathione peroxidase activities decreased in model group compared with those in normal group. Nuclear factor erythroid 2-related factor 2, heme oxygenase-1 and NAD(P)H quinone oxidoreductase 1 protein expressions were higher in low and high dose groups than those in model group. Naringenin protects against retinal damage in diabetic rats probably by resisting oxidative damage and inhibiting retinal tissue apoptosis through regulating protein expressions of the nuclear factor erythroid 2-related factor 2/antioxidant response element signaling pathway.