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

A. Zharikov, S. O. Filinova, O. Mazko, I. P. Bobrov, O. Makarova, A. Kalnitsky
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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.
卡诺辛对糖尿病实验中肾脏氧化损伤的影响
文章介绍了一项关于肌肽对实验性糖尿病肾脏氧化损伤的影响的研究结果。实验使用了两组 Wistar 大鼠:对照组(8 只)和实验组(11 只)。两组均模拟链脲佐菌素诱导的糖尿病,为期八周。从第 4 周到第 8 周,实验动物胃内注射肌肽(15 毫克/千克)。测定尿液中葡萄糖、蛋白质和肌酐的排泄浓度。八周结束时,取出大鼠的肾脏,测定氧化应激严重程度的指标(硫代巴比妥酸反应产物的浓度、总抗氧化活性、过氧化氢酶、超氧化物歧化酶、谷胱甘肽过氧化物酶的活性),并对肾小球的大小、肾小球血管床、毛细血管和间质的面积、荚膜细胞的数量进行形态测量。与对照组的比较显示,使用肌肽后,硫代巴比妥反应产物的浓度降低了 1.5 倍(p<0.001),总抗氧化活性提高了 2.2 倍(p<0.001),过氧化氢酶活性提高了 1.2 倍(p=0.039)。该组的肾小球和肾间质面积减少了 1.6 倍(p<0.001 和 p=0.04)。血流总面积增加了 2.4 倍(p<0.001),一根毛细血管的面积增加了 2.4 倍,肾小球中的荚膜细胞数量增加了 1.9 倍(p<0.001 和 p=0.001)。尿液中的蛋白质浓度也下降了 3.5 倍(p=0.007)。因此,在实验性糖尿病中,肌肽抑制高级糖化终产物的形成可减轻对肾脏的氧化损伤。蛋白尿的减少、荚膜细胞数量的增加、肾小球面积的缩小以及肾小球血管系统状况的改善都证明了这一点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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