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氨基胍对慢性束缚应激大鼠视觉诱发电位(VEP)、抗氧化状态及脂质过氧化的影响。

Effect of aminoguanidine on visual evoked potentials (VEPs), antioxidant status and lipid peroxidation in rats exposed to chronic restraint stress.

作者信息

Akpinar Deniz, Yargicoglu Piraye, Derin Narin, Aslan Mutay, Agar Aysel

机构信息

Akdeniz University, Faculty of Medicine, Department of Biophysics, Arapsuyu, Antalya, Turkey.

出版信息

Brain Res. 2007 Dec;1186:87-94. doi: 10.1016/j.brainres.2007.09.066. Epub 2007 Oct 4.

Abstract

The purpose of the study was to investigate the effect of aminoguanidine (AG) on visual evoked potentials (VEPs), thiobarbituric acid reactive substances (TBARS), the activities of Cu, Zn superoxide dismutase (Cu,Zn-SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), and nitrite/nitrate levels. Forty healthy male Wistar rats, aged 3 months, were divided into four equal groups: Control (C), the group treated with aminoguanidine (A), the group exposed to restraint stress (S), the group exposed to restraint stress and treated with aminoguanidine (AS). Chronic restraint stress was applied for 21 days (1 h/day) and aminoguanidine (50 mg/kg/day) was injected intraperitoneally to the A and AS groups for the same period. Aminoguanidine treatment significantly decreased retina and brain TBARS levels in rats exposed to restraint stress compared to rats exposed to restraint stress alone. Aminoguanidine treatment produced a significant decrease in brain and retina nitrite and nitrate levels with respect to the control groups. Aminoguanidine increased all antioxidant enzyme activities in both brain and retina in rats exposed to restraint stress compared to rats exposed to restraint stress alone. All VEP components were significantly decreased in AG treated rats exposed to restraint stress compared to rats exposed to restraint stress alone. Our study clearly showed that AG has the potential to prevent changes caused by stress.

摘要

本研究的目的是探讨氨基胍(AG)对视诱发电位(VEP)、硫代巴比妥酸反应性物质(TBARS)、铜锌超氧化物歧化酶(Cu,Zn-SOD)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)的活性以及亚硝酸盐/硝酸盐水平的影响。40只3个月大的健康雄性Wistar大鼠被分为四组,每组数量相等:对照组(C)、氨基胍治疗组(A)、束缚应激组(S)、束缚应激并氨基胍治疗组(AS)。慢性束缚应激持续21天(每天1小时),在此期间,A组和AS组腹腔注射氨基胍(50毫克/千克/天)。与单纯束缚应激的大鼠相比,氨基胍治疗显著降低了束缚应激大鼠视网膜和脑内的TBARS水平。与对照组相比,氨基胍治疗使脑和视网膜中的亚硝酸盐和硝酸盐水平显著降低。与单纯束缚应激的大鼠相比,氨基胍增加了束缚应激大鼠脑和视网膜中所有抗氧化酶的活性。与单纯束缚应激的大鼠相比,在接受氨基胍治疗的束缚应激大鼠中,所有VEP成分均显著降低。我们的研究清楚地表明,AG有可能预防应激引起的变化。

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