Diabetic retinopathy is a progressive tissue-specific neurovascular complication of diabetes with a multifactorial pathogenesis, in which microvascular disorders are preceded by damage to nerve elements. The latter begin with the early involvement of glia, including astrocytes and Müller cells. Taking into account the establishment of GABA-ergic deficiency, the use of modulators of the GABA-benzodiazepine receptor complex, for example, Carbacetam, which has shown satisfactory neuroprotective properties, seems promising. Diabetes mellitus was modeled by a single administration of streptozotocin (50 mg/kg; “Sigma-Aldrich”, China) to threemonth-old male Wistar rats. Already after 7 days, according to immunohistochemical detection of glial fibrillary acidic protein (GFAP), reactive gliosis of astrocytes of the inner retina layers was detected, to which Müller cells joined from the 14th day. The content of GFAP in retinal tissues increased significantly. GFAP-positive cells were in close contact with foci of pathological angiogenesis in the inner layers of the retina and also took part in the formation of fibrous proliferates in the outer layers. Detection of caspase-3 showed the activation of apoptosis in astrocytes and radial processes of Müller cells in the inner plexiform layer. Carbacetam in combination with insulin reduced the expression of GFAP and caspase-3 in the retina and prevented the development of reactive gliosis, angiogenesis, and the formation of fibrous proliferates, which makes it a candidate for further studies in the treatment of diabetic retinopathy.