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哇巴因对躁狂症动物模型中细胞因子/趋化因子水平的影响。

Effects of ouabain on cytokine/chemokine levels in an animal model of mania.

作者信息

Tonin Paula T, Valvassori Samira S, Lopes-Borges Jéssica, Mariot Edemilson, Varela Roger B, Teixeira Antônio Lucio, Quevedo João

机构信息

Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde (PPGCS), Unidade Acadêmica de Ciências da Saúde (UNASAU), Universidade do Extremo Sul Catarinense (UNESC), Criciúma, SC, Brazil.

Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde (PPGCS), Unidade Acadêmica de Ciências da Saúde (UNASAU), Universidade do Extremo Sul Catarinense (UNESC), Criciúma, SC, Brazil.

出版信息

J Neuroimmunol. 2014 Nov 15;276(1-2):236-9. doi: 10.1016/j.jneuroim.2014.09.007. Epub 2014 Sep 17.

DOI:10.1016/j.jneuroim.2014.09.007
PMID:25288301
Abstract

Bipolar disorder (BD) is a chronic and severe psychiatric disorder and despite its importance, little is known about the precise pathophysiology of this disorder. Several studies have reported that inflammation plays a role in the pathogenesis of BD and that cytokines are altered in these patients. Intracerebroventricular (ICV) injection of ouabain (a potent Na(+)/K(+)-ATPase inhibitor) in rats resulted in manic-like effects and it has been widely used as an animal model of bipolar mania. In this study, we assessed the cytokine levels (IL-1β, IL-6, IL-10, TNF-α, CINC-1) in the brain structures (hippocampus, striatum, frontal cortex, amygdala), serum and cerebrospinal fluid (CSF) of rats submitted to an animal model of mania induced by ouabain. Our findings demonstrated that ouabain induced hyperlocomotion in rats. However, the only cytokine that showed alteration was IL-6, which was decreased in the striatum after ouabain administration. In conclusion, despite the ouabain administration in rats be a valid model to study the physiopathology of bipolar mania, it seems that this model was not able to mimic the changes in cytokines observed in bipolar patients.

摘要

双相情感障碍(BD)是一种慢性严重精神疾病,尽管其很重要,但对该疾病的确切病理生理学知之甚少。多项研究报告称,炎症在BD的发病机制中起作用,且这些患者体内细胞因子发生了改变。给大鼠脑室内(ICV)注射哇巴因(一种有效的钠钾ATP酶抑制剂)会导致类似躁狂的效应,它已被广泛用作双相躁狂的动物模型。在本研究中,我们评估了接受哇巴因诱导的躁狂动物模型的大鼠脑结构(海马体、纹状体、额叶皮质、杏仁核)、血清和脑脊液(CSF)中的细胞因子水平(IL-1β、IL-6、IL-10、TNF-α、CINC-1)。我们的研究结果表明,哇巴因可诱导大鼠活动过度。然而,唯一显示有变化的细胞因子是IL-6,在给予哇巴因后纹状体中的IL-6水平降低。总之,尽管给大鼠注射哇巴因是研究双相躁狂病理生理学的有效模型,但该模型似乎无法模拟双相情感障碍患者中观察到的细胞因子变化。

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