Diabetic retinopathy (DR) is the most common microvascular complication in patients with diabetes and a leading cause of vision loss. Recent studies have shown that inflammation and oxidative stress play central roles in its development and progression. Hyperglycemia activates systemic immune cells and retinal resident cells, inducing the release of various inflammatory mediators and chemokines, which disrupt the blood-retinal barrier, leading to capillary leakage and neurodegenerative changes. Meanwhile, the positive feedback loop between inflammation and reactive oxygen species/nitric oxide further amplifies pathological damage, explaining the limited efficacy of anti-vascular endothelial growth factor monotherapy. Oxidative stress manifests as the excessive generation of free radicals such as reactive oxygen species due to hyperglycemia, directly damaging retinal cells and activating inflammatory signaling pathways, thereby exacerbating vascular damage and neurodegeneration. Future therapeutic strategies should adopt multi-target and multi-link interventions, with particular emphasis on the combined application of anti-inflammatory and antioxidant treatments, such as immunomodulation, macrophage phenotype regulation, intervention in the neutrophil extracellular trap axis, and combination therapy using anti-vascular endothelial growth factor drugs and antioxidants, to more effectively intervene in the pathological progression of DR.