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당뇨 유발 백서에서 aminoguanidine의 항산화 작용
임자혜,김진범 경기대학교 2000 論文集 Vol.44 No.2
Oxidative stress is defined as an oxidative damage caused by reactive oxygen or oxygen radicals in a biological system. In diabetes, oxidative stress is known to be increased and is implicated in the pathogenesis of diabetic complications. Hyperglycemia in diabetes causes increase formation of Amadori products, which in turn form advanced glycosylation end products(AGEs). It has been proposed that formation of distortion of subcellular structures, resulting in irreversible tissue damage of diabetic complications. Recently, it has been reported that the interaction of AGEs with their cellular receptors induces reactive oxygen intermediates. Thus, it has been proposed that AGE contribute to the oxidative stress which has been hypothesized to underlie diabetic complications. Aminoguanidine(AG) is a prototype inhibitor of AGE formation. The purpose of this study was to see whether the inhibition of formation of AGE by aminoguanidine administration could prevent or ameliorate the increased oxidative stress in streptozotocin(STZ)-induced diabetic rats. To pursue this, we performed a preliminary in vitro study and then in vivo study using a diabetic animal model. For in vitro study, we observed the effect of AG on an inhibition of in vitro AGE formation, and, in addition, its effect on lowering the degree of lipid peroxidation employing phospholipid liposome and LDL as a model system. In vitro study showed that in the presence of 10mM AG, AGE formation was reduced by 50.6% compared with control. Besides, the lipid peroxdation in phospholipid liposome and LDL, judged by the concentration of TBARS, was decreased markedly in the presence AG in a dose-dependent manner. For in vivo study, Sprague Dawley rats were divided into three groups, group Ⅰ(non-diabetic control), group Ⅱ(STZ-induced diabetic) and group Ⅲ(AG-fed diabetic), and twelve weeks later, plasma glucose and cholesterol content, the amount of AGEs in plasma and the extent of lipid peroxidation in plasma, kidney, liver and heart were measured. The blood glucose and cholesterol levels of group Ⅱ and group Ⅲ were not significantly different showing that aminoguanidine did not affect those. The plasma AGE concentration was increased in diabetic control group by 32.7% than that of nondiabetic control and AG-feeding lowered it by 26.1%. The MDA concentrations in kidney, liver and heart tissue were increased in group Ⅱ by 34%, 48% and 22%, respectively, compared to group Ⅰ, and AG-feeding had an effect in reducing those by 8%, 19% and 14%, respectively than diabetic control. In conclusion, we observed that the inhibition of AGE formation by aminoguanidine administration resulted in the decrease of enhanced lipid peroxidation in diabetic rats. This amelioration of oxidative stress by pharmacologic inhibition of AGE formation in STZ-induced diabetic rats suggests that aminoguanidine have a potential therapeutic role in the treatments of diabetic patients.
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Streptozotocin 유발성 당뇨백서에서 해당효소에 대한 Phlorizin의 효과
배학연,정회상,박유환,전용준,이승일,문철웅,양성훈,이병래 朝鮮大學校 附設 醫學硏究所 1991 The Medical Journal of Chosun University Vol.15 No.1
In glycolysis, the reactions catalyzed by hexokinase, Phosphofructokinase, and pyruvate kinase are lally irreversible; hence they would be expected to have regulatory as well as catalytic roles. They ilso adaptive in a number of physiological states, and although the molecular mechanisms controlling adaptations are largely unknown, dietary and hormonal stimuli serve as environmental factors lating enzyme levels in vivo. The present study was undertaken to examine the effects of phlorizin, a blocker of renal tubular ose reabsorption, on the activities of glucokinase, hexokinase, and pyruvate kinase in the liver and nrocytes of streptozotocin (STZ) diabetic rats. The levels of plasma glucose and insulin and the activities of glycolytic enzymes were measured onchird day after phlonzin treatment in normal and STZ diabetic rats and the results were as follows. 1. Plasma glucose levels were reduced by 14.35%(P<0.05) in normal rats and by 39.38% (p<0.01) in STZ diabetic rats. 2. Plasma insulin levels were reduced by 45.6% (P<0.05) in normal rats and by 58.2% (P<0.01) in STZ diabetic rats. 3. On the third day after phlorizin treatment, hepatic glucokinase and pyruvate kinase activities in normal rats were reduced by approximately 56% (P<0.01) and 43% (P<0.01) respectively, and erythrocyte hexokinase and pyruvate kinase activities were reduced by approximately 18% (P<0.05) and 22% (P<0.01) respectively, In STZ diabetic rat shepatic glucokinase and pyruvate kina activities were reduced by approximately 52% (P<0.01) and 22% (P<0.01) respectively, a erythrocyte hexokmase and pyruvate kinase activities were reduced by approximately 4% and 3 respectively. Thus the overall decreases of the levels of plasma glucose and insulin and the activity of glycoly enzymes were observed on the third day after phlorizin treatment in normal and STZ diabetic ra These alterations in the enzyme activity with phlorizin treatment were shown to be a result of reducinsulin levels, and the smaller decrease in enzyme actvity in STZ diabetic rats than in normal rats thought to be probably due to the reduced response to changes in insulin levels at near basal levels enzyme activity.
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