Effect of Carnosine on Oxidative Damage to the Kidneys in Experinental Diabetes Mellitus

Author:

Zharikov A. Yu.1,Filinova S. O.1,Mazko O. N.1,Bobrov I. P.1,Makarova O. G.1,Kalnitsky A. S.1

Affiliation:

1. Altai State Medical University of the Ministry of Health Care of the Russia

Abstract

The article presents the results of a study into the effect of carnosine on oxidative damage to the kidneys in experimental diabetes mellitus. The experiment was carried out using two groups of Wistar rats: control (n=8) and experimental (n=11). In both groups, streptozotocin-induced diabetes mellitus was simulated for eight weeks. Experimental animals were intragastrically injected with carnosine (15 mg/kg) from weeks 4 to 8. The concentration of glucose, protein and creatinine excretion in urine were determined. At the end of eight weeks, the kidneys were removed from the rats to determine the indicators of oxidative stress severity (concentration of thiobarbiturate-reactive products, total antioxidant activity, activity of catalase, superoxide dismutase, glutathione peroxidase) and to conduct morphometry of the size of the renal glomeruli, the area of the vascular bed, capillaries and mesangium in the glomeruli, the number of podocytes. A comparison with the control showed the use of carnosine led to a 1.5-fold decrease in the concentration of thiobarbiturate-reactive products (p<0.001), a 2.2-fold increase in the total antioxidant activity (p<0.001), and a 1.2-fold increase in catalase activity (p=0.039). The area of the renal glomeruli and the mesangium in this group decreased by 1.6 times (p<0.001 and p=0.04, respectively). The total area of blood flow increased by 2.4 times (p<0.001), the area of one capillary, and the number of podocytes in the glomerulus increased by 1.9 times (p<0.001 and p=0.001). A 3.5-fold decrease in protein concentration in urine was also noted (p=0.007). Therefore, inhibition of the formation of advanced glycation end products by carnosine in experimental diabetes mellitus attenuates oxidative damage to the kidneys. This is evidenced by a decrease in proteinuria, an increase in the number of podocytes, a decrease in the area of the renal glomeruli, and an improvement in the condition of the glomerular vascular system.

Publisher

Scientific Center for Biomedical Technologies of the Federal Medical-Biological Agency

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