四氧嘧啶诱导的糖尿病大鼠脑内氧化应激增加和抗氧化酶失衡。

Experimental Diabetes Research Pub Date : 2012-01-01 Epub Date: 2012-05-08 DOI:10.1155/2012/302682
Luciane B Ceretta, Gislaine Z Réus, Helena M Abelaira, Karine F Ribeiro, Giovanni Zappellini, Francine F Felisbino, Amanda V Steckert, Felipe Dal-Pizzol, João Quevedo
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引用次数: 83

摘要

糖尿病(DM)与中枢神经系统(SNC)的病理改变以及氧化应激的改变有关。因此,本研究的主要目的是评估四氧嘧啶诱导的糖尿病动物模型对记忆和氧化应激的影响。采用单次注射四氧嘧啶(150 mg/kg)诱导Wistar大鼠糖尿病,诱导15 d后采用物体识别任务评价大鼠记忆。测定大鼠脑内氧化应激参数及抗氧化酶、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性。结果显示,糖尿病大鼠的识别记忆没有改变。然而,研究结果确实表明,糖尿病大鼠前额叶皮层的超氧化物水平以及前额叶皮层和杏仁核亚线粒体颗粒中硫代巴比妥酸活性物质(TBARS)的产生有所增加。此外,海马和纹状体的蛋白质氧化增加,纹状体和杏仁体的TBARS氧化增加。糖尿病大鼠纹状体和杏仁核SOD活性降低。然而,在糖尿病大鼠的海马中,CAT活性增加。综上所述,我们的研究结果表明,四氧嘧啶诱导的糖尿病动物模型没有引起动物识别记忆的改变,但它产生了氧化剂,使SOD和CAT活性失衡,这可能有助于糖尿病的病理生理。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Increased oxidative stress and imbalance in antioxidant enzymes in the brains of alloxan-induced diabetic rats.

Increased oxidative stress and imbalance in antioxidant enzymes in the brains of alloxan-induced diabetic rats.

Increased oxidative stress and imbalance in antioxidant enzymes in the brains of alloxan-induced diabetic rats.

Increased oxidative stress and imbalance in antioxidant enzymes in the brains of alloxan-induced diabetic rats.

Diabetes Mellitus (DM) is associated with pathological changes in the central nervous system (SNC) as well as alterations in oxidative stress. Thus, the main objective of this study was to evaluate the effects of the animal model of diabetes induced by alloxan on memory and oxidative stress. Diabetes was induced in Wistar rats by using a single injection of alloxan (150 mg/kg), and fifteen days after induction, the rats memory was evaluated through the use of the object recognition task. The oxidative stress parameters and the activity of antioxidant enzymes, superoxide dismutase (SOD), and catalase (CAT) were measured in the rat brain. The results showed that diabetic rats did not have alterations in their recognition memory. However, the results did show that diabetic rats had increases in the levels of superoxide in the prefrontal cortex, and in thiobarbituric acid reactive species (TBARS) production in the prefrontal cortex and in the amygdala in submitochondrial particles. Also, there was an increase in protein oxidation in the hippocampus and striatum, and in TBARS oxidation in the striatum and amygdala. The SOD activity was decreased in diabetic rats in the striatum and amygdala. However, the CAT activity was increased in the hippocampus taken from diabetic rats. In conclusion, our findings illustrate that the animal model of diabetes induced by alloxan did not cause alterations in the animals' recognition memory, but it produced oxidants and an imbalance between SOD and CAT activities, which could contribute to the pathophysiology of diabetes.

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来源期刊
Experimental Diabetes Research
Experimental Diabetes Research 医学-内分泌学与代谢
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