https://doi.org/10.31288/oftalmolzh201524954

The possibility of correcting violations of glycolytic processes in the retina using quercetin and lipoate with streptozotocin diabetes 

O. A. Moroz 

SI «Filatov Institute of Eye Diseases and Tissue Therapy of the National Academy of Medical Science of Ukraine»; Odessa (Ukraine) 

The Zakarpatye Regional Clinical Hospital named after. A. Nowak; Uzhgorod (Ukraine)Introduction.

Relevance of the work is to study the effect of quercetin and lipoate in the treatment of experimental diabetes. 

Purpose. Explore the possibility of correcting violations of glycolytic processes in the retina using quercetin and lipoate with streptozotocin diabetes. 

Methods. Studies were conducted on 55 white rats. Experimental animals were divided into four groups: first — control group (14 rats), the second — experimental group (14 rats), animals with diabetes, without the use of drugs, the third — the experimental group (12 rats), animals with diabetes, and the use of lipoic acid, Results. In the context of the application of lipoic acid and quercetin metabolites showed a decrease carbohydrate-phosphorus metabolism in the retina and the blood of experimental animals with streptozotocin diabetes. 

Conclusion. 1. The test drug prevents the degree of violation redox processes in the retina. This was confirmed by a decrease in lactate and pyruvate concentrations in the retina in diabetic animals in the study drugs application (bioflavonoid — quercetin and thiol preparation — lipoate). 2. The most pronounced protective effect on the degree of violation of anaerobic and aerobic glucose oxidation in retina characteristic of lipoic acid. 3. Study drug (bioflavonoid — quercetin and thiol compound — lipoic acid) showed its positive metabolic effect and at the system level. Thus, after 6 months of the experiment under the influence of lipoic acid lactate levels decreased by 37.6 % and pyruvate — 26.2 %, and the quercetin when exposed to lactate was reduced by 35.3 % and pyruvate — 22, 7 % compared to diabetic animals without drug experimentthe fourth — the experimental group (15 rats), animals with diabetes and the use of quercetin. In retinas homogenates and plasma produced determination of pyruvate and lactate. 

Key words: streptozotocin diabetes, retina, glycolytic processes, correction, 

References 

1. Aleksandrovskii AYa. Molecular mechanisms of development of diabetic complications. Biokhimiia. 1998;63(11): 1470–9. In Russian. 
2. Yefimov A, Skorobronskaia N, Zuieva N. Diabetic neuropathy. Liky Ukrainy. 2005;3:21–5. In Russian. 
3. Leus NF. Metabolic mechanisms of development and prospects of medical treatment of diabetic retinopathy. Oftalmol Zh. 2003;5:75–80. In Russian. 
4. Nasledov A. SPSS computer analysis of data in psychology and social sciences. Spb.:Piter; 2005. 416 p. 
5. New methods of biochemical analysis. Izd. Leningradskogo univer; 1991. 395 p. 
6. Oleinik TV, Kolomiichuk SG, Baidan EI. Influence of coenzyme functionally related to the level of key metabolites of carbohydrate-phosphorus metabolism in the retina of rats with streptozotocin diabetes. Oftalmol Zh. 2006;1:50–3. In Russian. 
7. Pasyechnikova NV, Naumenko AV, Zborovskaia AV. The state of the blood retinal barrier in diabetic retinopathy according fluorometry. Oftalmopl Zh. 2008;5:4–7. In Russian. 
8. Pasyechnikova NV. Laser treatment of the pathology of the fundus. Kyiv: NAukova Dumka; 2007. 201 p. 
9. Poltorak VV, Blokh KO, Malashenko AM. Experimental modeling of diabetes to study the specific effect of new antidiabetic agents. Metodological recommendations. Kharkov; 1991. 19 p. 
10. Barber A J. A new view of diabetic retinopathy: a neurodegenerative disease of the eye. Prog. In Neuro-Psychopharm. & Biol. Psych. 2003; 27:283–90. 
    Crossref   Pubmed
11. Barber AJ, Robinson WF. Neurodegeneration in Diabetic Retinopathy. Visual Dysfunction in Diabetes Ophthalmol. Res. 2012;45:189–209. 
    Crossref 
12. Bergamini CM, Gambetti S, Dondi A. Oxygen, reactive oxygen species and tissue damage. Cur.Pharm. Design. 2004;10(14):1611–26. 
    Crossref   Pubmed
13. Bergmeyer HU. Methoden der enzymatischen Analyse. Herausgegeben von H. U. Bergmeyer. Berlin. 1986; 2220 p. 
14. Bloomgarden ZT. Diabetic retinopathy and diabetic neuropathy. J. Diabetes Care. 2007;30(3):760–5. 
15. Brownlee M. The pathobiology of diabetic complications (a unifying mechanism). J. Diabetes. 2005;54:1615–25. 
16. Fosmark DS, Torjesen PA, Kilhovd BK. Increased serum levels of the specific advanced glycation end product methylglyoxal-derived hydroimidazolone are associated with retinopathy in patients with type 2 diabetes mellitus. Metabolism. 2006;55:232–6. 
17. Kowluru RA, Chan PS. Oxidative stress and diabetic retinopathy. Exp. Diabet. Res. 2007. 12 p. 
18. Lorenzi M, Gerhardinger C. Early cellular and molecular changes induced by diabetes in the retina. Diabetologia. 2001;44:791–804. 
19. Obrosova IG, Drel VR, Kumagai AK. Early diabetes-induced biochemical changes in the retina: comparison of rat and mouse models. Diabetologia. 2006; 49:2525–33. 
20. Rabbani N, Thornaley PJ. The Critical Role of Methylglyoxal and Glyoxalase 1 in Diabetic Nephropathy. Diabetes. 2014;63:50–2. 
21. Simo S, Hernandez C. Neurodegeneration in the diabetic eye: new insights and therapeutic perspectives. Trends in Endocrinology and Metabolism. 2014;25: 23–33. 
    Crossref   Pubmed