Electrophysiological characteristics of experimental diabetes under the conditions of using niacin-oxy-ethylidene-diphosphonate germinate (MIGU-4)

Abstract

Diabetic retinopathy occupies the second leading cause of visual impairments and blindness all over the world. Oxidative stress contributes to diabetes-induced retinopathy and visual pathway deterioration as well. Determining compounds with heightened antioxidant potential involves increasing the effectiveness of diabetes complications treatment. Recently, it has been established that germanium-containing organic compounds possess antioxidative and neuroprotective activity. Hence, the estimation of retinopathy manifestations on a streptozotocin (STZ)-induced rodent model, which is one of the most commonly employed models in preclinical drug research for diabetic retinopathy under conditions of niacin-oxy-ethylidene-diphosphonate germanate (MIGU-4) treatment, is justified. The dynamics of visual evoked potential (VEP) and the comparison with the effects of α-tocopherol obtained in streptozotocin (STZ)-induced diabetes in Wistar rats were the objectives of the work. Treatment with MIGU-4 (25.0 mg/kg, i.p.) and α-tocopherol (100.0 mg/kg, i.p.) started one week after STZ administration (65.0 mg/kg, i.p.).and was performed daily with the measurement of VEP characteristics for six and twelve weeks. Intact and STZ-diabetes rats treated with 0.9% NaCl solution were observed as separate groups. The latency of P1, N1, and P2 in STZ-treated rats significantly exceeded corresponding indices in the control animals, and the amplitude of P1-N1 and N1-P2 was reduced in six and twelve weeks from the moment of STZ administration. Treatment with MIGU-4 six weeks after STZ resulted in a significant shortening of the P1 and N1 latency compared with the diabetes rats and heightened amplitude of waves. The latency of VEP waves in α-tocopherol treated rats did not differ from the control. MIGU-4 treatment twelve weeks after STZ significantly shortened the latency of P1 compared with the diabetes rats. The amplitude of VEP waves was not affected by MIGU-4, and α-tocopherol treatment failed to prevent diabetes-induced VEP deterioration in the twelve weeks after STZ. The conclusion was made that MIGU-4 (25.0 mg/kg) causes protection against enlargement of VEP wave latency and reduced amplitude in rats with STZ diabetes. The protective effect was more pronounced at the early stage of STZ-diabetes development (six weeks) and exceeded that caused with α-tocopherol (100.0 mg/kg) treatment. Further investigations of MIGU-4 in the complex treatment of diabetes retinopathy are in prospect.