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慢性变应原应激导致大鼠血液氧化应激和丁酰胆碱酯酶活性降低。

Chronic variable stress induces oxidative stress and decreases butyrylcholinesterase activity in blood of rats.

机构信息

Laboratório de Neuroproteção e Doenças Metabólicas, Departamento de Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul, UFRGS, Rua Ramiro Barcelos, 2600-Anexo, Porto Alegre, RS, CEP 90035-003, Brazil.

出版信息

J Neural Transm (Vienna). 2010 Sep;117(9):1067-76. doi: 10.1007/s00702-010-0445-0. Epub 2010 Aug 5.

DOI:10.1007/s00702-010-0445-0
PMID:20686907
Abstract

Depressive disorders, including major depression, are serious and disabling, whose mechanisms are not clearly understood. Since life stressors contribute in some fashion to depression, chronic variable stress (CVS) has been used as an animal model of depression. In the present study we evaluated some parameters of oxidative stress [thiobarbituric acid reactive substances (TBARS), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx)], and inflammatory markers (interleukin 6, C reactive protein, tumor necrosis factor-alpha and nitrites), as well as the activity of butyrylcholinesterase in blood of rats subjected to chronic stress. Homocysteine and folate levels also were measured. Stressed animals were submitted to different mild stressors for 40 days. After CVS, a reduction in weight gain was observed in the stressed group, as well as an increase in immobility time in the forced swimming test as compared with controls. Stressed animals presented a significant increase on TBARS and SOD/CAT ratio, but stress did not alter GPx activity and any inflammatory parameters studied. CVS caused a significant inhibition on serum butyrylcholinesterase activity. Stressed rats had higher plasmatic levels of homocysteine without differences in folate levels. Although it is difficult to extrapolate our findings to the human condition, the alterations observed in this work may be useful to help to understand, at least in part, the pathophysiology of depressive disorders.

摘要

抑郁障碍,包括重度抑郁症,是严重且致残的疾病,其发病机制尚不清楚。由于生活应激源以某种方式促成了抑郁的发生,慢性可变应激(CVS)已被用作抑郁的动物模型。在本研究中,我们评估了一些氧化应激参数[硫代巴比妥酸反应物质(TBARS)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)]以及炎症标志物(白细胞介素 6、C 反应蛋白、肿瘤坏死因子-α和亚硝酸盐),以及接受慢性应激的大鼠血液中丁酰胆碱酯酶的活性。还测量了同型半胱氨酸和叶酸水平。应激动物接受了 40 天的不同轻度应激。在 CVS 后,与对照组相比,应激组动物体重增加减少,强迫游泳试验中的不动时间增加。应激动物的 TBARS 和 SOD/CAT 比值显著增加,但应激并未改变 GPx 活性和研究的任何炎症参数。CVS 导致血清丁酰胆碱酯酶活性显著抑制。应激大鼠的血浆同型半胱氨酸水平升高,但叶酸水平没有差异。尽管很难将我们的发现外推到人类疾病中,但本工作中观察到的改变可能有助于至少部分理解抑郁障碍的病理生理学。

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