Diabetes is currently considered a non-infectious epidemic. At the same time the main reason for the development of blindness in developed countries are pathological changes in blood vessels in eye diseases, primarily in diabetic retinopathy. The purpose of the study: analysis of changes in secondary products of lipid peroxidation in experimental diabetic retinopathy and in different ways of its correction. The study was performed on white Wistar rats weighing 180-200 g. According to the tasks, the animals were divided into 7 groups. Type 2 diabetes mellitus and diabetic retinopathy were simulated by intraperitoneal administration of streptozotocin (Sigma, USA) dissolved in 0.1 M citrate buffer with a pH of 4.5. The dose of streptozotocin 55 mg / kg body weight was divided into two injections. The introduction of streptozotocin was preceded by a high-fat diet for 28 days. Corrective agents used in the study: metformin, aflibercept, L-carnitine, bromfenac, L-arginine and citicoline. The results obtained indicate an increase in the activity of lipid peroxidation, starting from the 30th and with subsequent progression to the sixtieth and one hundred and eightieth days of experimental diabetic retinopathy. This is confirmed by the increase in the level of malondialdehyde in the 2nd group, the maximum of which is observed at the third stage. Correction with hypoglycemic agents in the 3rd group had a positive effect, but was not able to reduce the level of secondary products of lipid peroxidation, so it became necessary to use additional agents. The use of aflibercept and a nitric oxide donor in the 4th group to correct the development of diabetic retinopathy significantly inhibited oxidative stress, the maximum of which occurred on the one hundred and eightieth day of the experiment, but did not reach the control values. It was proved that the combined administration of bromfenac and aflibercept in the 5th group significantly reduced the amount of LPO secondary products, but not as significantly as in the 4th group. It was proved that the administration of aflibercept, L-carnitine and bromfenac to animals of the 6th group reduced the content of LPO secondary products already on the 30th day and was prolonged on the 60th and 180th days of the study, but did not reach the control values ​​either. The most effective correction was the combination of metformin, aflibercept, L-arginine and citicoline in rats of the 7th group, as evidenced by the normalization of the level of malondialdehyde on the thirtieth and sixtieth days of the experiment, and on the one hundred and eightieth a decrease in the content of the marker to the control values ​​was recorded.

To date, the key role of endothelial dysfunction in the occurrence and progression of diabetes mellitus and diabetic retinopathy has been proven. The study was performed on white Wistar rats weighing 180-200 g. According to the tasks, the animals were divided into 7 groups. Our results indicate a violation of vasodilation on the 30th day of experimental diabetic retinopathy with subsequent progression of pathological changes on the 60th and 180 th day of the study, as evidenced by a decrease in the content of S-nitrosothiols in group 2 (p <0,001), most pronounced in the 3 rd stage. When analyzing the data of group № 3, it was found that the correction of the pathological condition with the help of hypoglycemic agents (correction of hyperglycemia, aflibercept, L-arginine and citicoline solution) more pronouncedly normalizes the content of the vasodilation marker compared to other groups of our experiment, which is pronounced in long-term correction-on 180 th day.

The article presents the results of an experimental study of the AOР and LPО system in animals simulated complications of the microcirculatory tract (diabetic retinopathy, diabetic nephropathy) on the background of type 2 diabetes. It was found that in the group of animals with type 2 diabetes increased the level of DC, TBCproducts and MDA; catalase and FG levels decreased. In animals with simulated DN, AOP disorders were more pronounced compared to animals with DR. This trend can be explained by the fact that in addition to hyperglycemia in these animals, the excessive formation of free radicals contributes to metabolic shifts in ischemic areas of tissues and organs. Disturbance of balance in AOP and LPO in type 2 diabetes triggers a pathogenetic cascade of development of complications of the microcirculatory tract and is accompanied by a tendency to further increase the generation of reactive oxygen species and activation of POL in microangiopathies.

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