Abstract
Background. In the development of diabetic retinopathy (DR), an important role belongs to the signaling pathways of cellular protein kinases, which implement the effects of external factors. Their blockade is a reasonable measure to prevent the development of DR, which, probably, can be implemented through inhibition of the pro-inflammatory role of retinal microglia. Aim: to study the state of retinal microglia by the content of Iba-1 and CD68 expression in experimental DR and the effect of the use of the cellular protein kinase blocker Sorafenib. Materials and methods. In male Wistar rats, DR was modeled by a single injection of streptozotocin (50 mg/kg; SigmaAldrich, Co, China). Rats were divided into 3 groups: control, with the introduction of Insulin (30 U; NovoNordiskA/S, Bagsvaerd, Denmark) and with the introduction of Insulin and Sorafenib (50 mg/kg; Сipla, India). Immunohistochemical study was performed using monoclonal antibodies against CD68 (Clone KP-1, Master Diagnostica, Spain). Determination of the content of Iba-1 in retinal tissue lysates was performed by immunoblotting (Invitrogen, USA). Results. Seven days after streptozotocin administration, CD68-positive staining was observed around the vessels in the choroid plexus, along the course of the vessels along the inner surface of the retina, and near the vessels of the inner plexiform layer. The number of stained elements and the intensity of staining increased after 28 days, and after 3 months, a large population of single CD68-positive cells appeared in the inner layers of the retina. The use of Insulin with Sorafenib significantly reduced CD68-positive staining of the retina. Iba-1 was not detected in retinal tissues of intact rats by immunoblotting, but under DR conditions its expression was at a high level. Trace concentrations of Iba-1 were detected with insulin treatment, while the marker was not detected with Insulin and Sorafenib. Conclusion. A decrease in the content of Iba-1 and expression of CD68 in the diabetic retina under the influence of Sorafenib was shown, which indicated the inhibition of early activation of microglia and resident monocytes during hyperglycemia