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Effects of sodium butyrate on oxidative stress and behavioral changes induced by administration of d-AMPH

机译:丁酸钠对d-AMPH诱导的氧化应激和行为改变的影响

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摘要

Several evidences have demonstrated that oxidative stress has a central role in bipolar disorder (BD). Recently, studies have been suggested histone deacetylases (HDAC) as a possible target for new medications in treatment of mood disorders. In this study, we investigated the effects of sodium butyrate (SB, a histone deacetilase inhibitor) on oxidative stress in rats submitted to an animal model of mania induced by d-amphetamine (d-AMPH). Wistar rats were first given d-AMPH or saline (Sal) for 14 days, and then, between days 8 and 14, rats were treated with SB or Sal. Locomotor activity and risk-taking behavior were assessed by open-field test and oxidative stress was measured in prefrontal cortex, amygdala, hippocampus and striatum. The results showed that SB reversed and prevented d-AMPH-induced behavioral effects. The d-AMPH administration induced oxidative damage in all brain structures analyzed. Depending on the cerebral area and technique, SB was able to reverse this impairment. The present study reinforces the need for more studies of HDAC inhibitors as possible target for new medications in treatment for BD.
机译:一些证据表明,氧化应激在双相情感障碍(BD)中具有重要作用。最近,研究表明组蛋白脱乙酰基酶(HDAC)可能是治疗情绪障碍的新药物的靶标。在这项研究中,我们调查了丁酸钠(组蛋白脱乙酰基酶抑制剂)对由d-苯异丙胺(d-AMPH)诱导的躁狂症动物模型的氧化应激的影响。首先给Wistar大鼠d-AMPH或生理盐水(Sal),持续14天,然后在第8天和第14天之间,用SB或Sal治疗大鼠。运动能力和冒险行为通过开放视野测试进行评估,并测量前额叶皮层,杏仁核,海马和纹状体的氧化应激。结果表明,SB逆转并阻止了d-AMPH诱导的行为影响。 d-AMPH给药在所有分析的脑结构中引起氧化损伤。根据大脑区域和技术,SB能够逆转这种损伤。本研究加强了对HDAC抑制剂作为BD治疗新药可能靶点的更多研究的需求。

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