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在躁狂症动物模型中,脑内注射脑源性神经营养因子可保护大鼠大脑免受哇巴因诱导的氧化应激损伤。

Intracerebral Administration of BDNF Protects Rat Brain Against Oxidative Stress Induced by Ouabain in an Animal Model of Mania.

作者信息

Valvassori Samira S, Arent Camila O, Steckert Amanda V, Varela Roger B, Jornada Luciano K, Tonin Paula T, Budni Josiane, Mariot Edemilson, Kapczinski Flávio, Quevedo João

机构信息

Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 88806-000, Criciúma, SC, Brazil,

出版信息

Mol Neurobiol. 2015 Aug;52(1):353-62. doi: 10.1007/s12035-014-8873-8. Epub 2014 Aug 28.

DOI:10.1007/s12035-014-8873-8
PMID:25164569
Abstract

Several studies have suggested that alterations in brain-derived neurotrophic factor (BDNF) and increased oxidative stress have a central role in bipolar disorder (BD). Intracerebroventricular (ICV) injection of ouabain (OUA) in rats alters oxidative stress parameters and decreases BDNF levels in the brain. In this context, the present study aims to investigate the effects of BDNF ICV administration on BDNF levels and oxidative stress parameters in brains of rats submitted to animal model of mania induced by OUA. Wistar rats received an ICV injection of OUA, artificial cerebrospinal fluid (ACSF), OUA plus BDNF, or ACSF plus BDNF. Locomotor activity and risk-taking behavior in the rats were measured using the open-field test. In addition, we analyzed the BDNF levels and oxidative stress parameters (TBARS, Carbonyl, CAT, SOD, GR, and GPx) in the frontal cortex and hippocampus of rats. The BDNF was unable to reverse the ouabain-induced hyperactivity and risk-taking behavior. Nevertheless, BDNF treatment increased BDNF levels, modulated the antioxidant enzymes, and protected the OUA-induced oxidative damage in the brain of rats. These results suggest that BDNF alteration observed in BD patients may be associated with oxidative damage, both seen in this disorder.

摘要

多项研究表明,脑源性神经营养因子(BDNF)的改变和氧化应激增加在双相情感障碍(BD)中起核心作用。向大鼠脑室内(ICV)注射哇巴因(OUA)会改变氧化应激参数并降低脑中BDNF水平。在此背景下,本研究旨在探讨向ICV注射BDNF对接受OUA诱导的躁狂症动物模型的大鼠脑中BDNF水平和氧化应激参数的影响。Wistar大鼠接受ICV注射OUA、人工脑脊液(ACSF)、OUA加BDNF或ACSF加BDNF。使用旷场试验测量大鼠的运动活动和冒险行为。此外,我们分析了大鼠额叶皮质和海马中的BDNF水平和氧化应激参数(硫代巴比妥酸反应物、羰基、过氧化氢酶、超氧化物歧化酶、谷胱甘肽还原酶和谷胱甘肽过氧化物酶)。BDNF无法逆转哇巴因诱导的多动和冒险行为。然而,BDNF治疗增加了BDNF水平,调节了抗氧化酶,并保护了大鼠脑中OUA诱导的氧化损伤。这些结果表明,在BD患者中观察到的BDNF改变可能与该疾病中均可见的氧化损伤有关。

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