Arent Camila O, Valvassori Samira S, Steckert Amanda V, Resende Wilson R, Dal-Pont Gustavo C, Lopes-Borges Jéssica, Amboni Rafaela T, Bianchini Guilherme, Quevedo João
Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806000, Brazil.
Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806000, Brazil.
J Psychiatr Res. 2015 Jun;65:71-9. doi: 10.1016/j.jpsychires.2015.04.011. Epub 2015 Apr 18.
Bipolar disorder (BD) is a severe psychiatric disorder associated with social and functional impairment. Some studies have strongly suggested the involvement of oxidative stress in the pathophysiology of BD. Paradoxal sleep deprivation (PSD) in mice has been considered a good animal model of mania because it induces similar manic-like behavior, as well as producing the neurochemical alterations which have been observed in bipolar patients. Thus, the objective of the present study was to evaluate the effects of the antioxidant agent's n-acetylcysteine (Nac) and/or deferoxamine (DFX) on behavior and the oxidative stress parameters in the brains of mice submitted to the animal model of mania induced by PSD. The mice were treated for a period of seven days with saline solution (SAL), Nac, DFX or Nac plus DFX. The animals were subject to the PSD protocol for 36 h. Locomotor activity was then evaluated using the open-field test, and the oxidative stress parameters were subsequently evaluated in the hippocampus and frontal cortex of mice. The results showed PSD induced hyperactivity in mice, which is considered a manic-like behavior. In addition to this, PSD increased lipid peroxidation and oxidative damage to proteins, as well as causing alterations to antioxidant enzymes in the frontal cortex and hippocampus of mice. The Nac plus DFX adjunctive treatment prevented both the manic-like behavior and oxidative damage induced by PSD. Improving our understanding relating to oxidative damage in biomolecules, and the antioxidant mechanisms presented in the animal models of mania are important in helping to improve our knowledge concerning the pathophysiology and development of new therapeutical treatments for BD.
双相情感障碍（BD）是一种与社会和功能障碍相关的严重精神疾病。一些研究强烈表明氧化应激参与了双相情感障碍的病理生理过程。小鼠的反常睡眠剥夺（PSD）被认为是一种良好的躁狂动物模型，因为它会诱发类似躁狂的行为，以及产生在双相情感障碍患者中观察到的神经化学改变。因此，本研究的目的是评估抗氧化剂N-乙酰半胱氨酸（Nac）和/或去铁胺（DFX）对接受PSD诱导的躁狂动物模型的小鼠行为和脑内氧化应激参数的影响。将小鼠用生理盐水（SAL）、Nac、DFX或Nac加DFX处理7天。动物接受36小时的PSD方案。然后使用旷场试验评估运动活动，随后在小鼠的海马体和额叶皮质中评估氧化应激参数。结果显示PSD诱导小鼠活动亢进，这被认为是一种类似躁狂的行为。除此之外，PSD增加了脂质过氧化和蛋白质的氧化损伤，同时导致小鼠额叶皮质和海马体中抗氧化酶的改变。Nac加DFX辅助治疗可预防PSD诱导的类似躁狂行为和氧化损伤。增进我们对生物分子氧化损伤以及躁狂动物模型中抗氧化机制的理解，对于帮助我们增进对双相情感障碍病理生理学和新治疗方法开发的认识非常重要。
