REACTIVE RETINAL GLIOSIS IN EXPERIMENTAL DIABETIC RETINOPATHY AND THE EFFECT OF INHIBITION OF CELLULAR PROTEIN KINASES

Aim: to determine the effect of the cellular protein kinase inhibitor sorafenib on the development of reactive retinal gliosis in experimental diabetic retinopathy. Materials and methods. Diabetic retinopathy was modeled in male Wistar rats by a single injection of streptozotocin (50 mg/kg; Sigma-Aldrich, Co, China). Rats were divided into 3 groups: control, with insulin administration (30 U; NovoNordiskA/S, Bagsvaerd, Denmark) and with insulin and sorafenib administration (55 mg/kg; Сipla, India). Immunohistochemical study was performed using monoclonal antibodies against GFAP (“ThermoFisher Scientific”, USA). Determination of GFAP content in retinal tissue lysates was performed by immunoblotting. Results. With the development of diabetic retinopathy, a progressive increase in GFAP expression was noted in astrocytes of the nerve fiber layer and Müller cells. The content of GFAP in retinal tissues also increased, which confirmed the development of reactive gliosis. Treatment of animals with insulin led to a lower intensity of GFAP-positive staining of cells and reduced the content of GFAP in the retina. The addition of sorafenib prevented diabetogenic reactive gliosis of the retina. Conclusions. Prevention of activation of astrocytes and Müller cells of the retina in experimental diabetic retinopathy indicated in favor of the possible use of this drug for the treatment of early stages of diabetogenic retinal damage.