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首页> 外文期刊>Journal of trace elements in medicine and biology: Organ of the Society for Minerals and Trace Elements (GMS) >The possible protective effects of vitamin E and selenium administration in oxidative stress caused by high doses of glucocorticoid administration in the brain of rats
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The possible protective effects of vitamin E and selenium administration in oxidative stress caused by high doses of glucocorticoid administration in the brain of rats

机译:维生素E和硒给施用在大鼠脑中高剂量糖皮质激素给药引起的氧化应激中的可能保护作用

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Acute exposure to high doses of glucocorticoids (GCs) may potentially increase the basal levels of reactive oxygen species (ROS) by altering the defence capacity against oxidative damage. Also, antioxidants may affect the oxidative breakdown of tissues. Therefore, the aim of this work was to determine the effects of dietary intake vitamin E and selenium (Se) on lipid peroxidat ion (LPO) as thiobarbituric acid reactive substances (TBARS) and on the antioxidative defence mechanisms in the brain of rats treated with high doses of prednisolone. Two hundred and fifty adult male Wistar rats were randomly divided into five groups. The rats were fed a normal diet, but groups 3, 4, and 5 received a daily supplement in their drinking water of 20 mg vitamin E, 0.3 mg Se, and a combination of vitamin E and Se, respectively, for 30 days. For 3 days subsequently, the control (group 1) was treated with a placebo, and the remaining 4 groups were injected intramuscularly with 100 mg/kg body weight (bw) prednisolone. After the last administration of prednisolone, 10 rats from each group were killed at 4, 8, 12, 24, and 48 h and the activities of enzymes selenium-glutathione peroxidase (Se-GSH-Px) and catalase (CAT), and the levels of reduced glutathione (reduced GSH) and TSARS in their brains were measured. Se-GSH-Px and CAT enzyme activities, and reduced GSH levels in the prednisolone treatment group (group 2) began to decrease gradually at 4 h (p 0.01, p 0.05, respectively), falling respectively to 60, 50, and 40% of the control levels by 24 h (p 0.001, p 0.01), and recovering to the control levels at 48 h. In contrast, prednisolone administration caused an increase in the brain TBARS, reaching up to six times the level of the control at 24 h (p 0.001). However, supplementation with vitamin E and Se had a preventive effect on the elevation of the brain TBARS and improved the diminished activities of antioxidative enzymes and the levels of reduced GSH. Therefore, the present study attempts to determine the sequence of cellular membrane damage in the brain of the rats after high doses GC administration and the possible roles in vivo of vitamin E and Se, and their combination.
机译:急性暴露于高剂量的糖皮质激素(GCS)可以通过改变防止氧化损伤的防御能力来增加反应性氧物种(ROS)的基础水平。此外,抗氧化剂可能影响组织的氧化分解。因此,这项工作的目的是确定膳食摄入维生素E和硒(LPO)对脂质过氧化物离子(LPO)作为硫碱尿酸反应性物质(TBAR)的影响,并在治疗大鼠脑中的抗氧化防御机制上高剂量的泼尼松龙。两百五十个成年雄性Wistar大鼠随机分为五组。将大鼠喂养正常饮食,但第3,4和5组分别在20mg维生素E,0.3mg SE的饮用水中获得每日补充剂,以及维生素E和SE的组合30天。随后3天,用安慰剂处理对照(第1组),将剩余的4基团用100mg / kg体重(bw)泼尼松龙注射肌肉注射。在最后一次施用泼尼松龙施用后,来自每组的10只大鼠在4,8,12,24和48小时中丧生,并酶硒 - 谷胱甘肽过氧化物酶(SE-GSH-PX)和过氧化氢酶(CAT)的活性。测定了谷胱甘肽(减少GSH)和其大脑中的TSARS的水​​平。 Se-GSH-PX和猫酶活性,泼尼松龙治疗组(第2组)中的GSH水平降低,开始逐渐在4小时(P <0.01,P <0.05)逐渐降低,分别为60,50和40%的40%的控制水平×24小时(P <0.001,P <0.01),并在48小时内恢复到对照水平。相反,泼尼松酮给药导致脑TBAR的增加,在24小时时达到对照水平的高达六倍(P <0.001)。然而,通过维生素E和SE的补充对脑TBAR的升高并改善了抗氧化酶的减少和降低的GSH水平的预防作用。因此,本研究试图在高剂量GC给药后确定大鼠脑中的细胞膜损伤的序列及维生素E和SE的体内可能的作用及其组合。

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