Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran; Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
Brain Res Bull. 2020 Nov;164:380-391. doi: 10.1016/j.brainresbull.2020.09.007. Epub 2020 Sep 14.
Cognitive function is impaired by increased consumption of a high-fat diet (HFD). Also, HFD consumption can alter hydrogen sulfide (HS) metabolism. HS is an important signaling molecule with antioxidant effects that regulates multiple functions in the brain. In the present study, we investigated the effect of sodium hydrosulfide (NaHS, an HS donor) on cognitive impairment and oxidative stress changes induced by HFD consumption. Following 11 weeks of HFD regimes in Wistar rats, elevated plus-maze (EPM), Morris water maze (MWM), and passive avoidance learning (PAL) tasks were used to evaluate the anxiety-like behavior and spatial and passive learning and memory, respectively. Daily intraperitoneal injection of NaHS was done during the dietary regimen. Serum and hippocampal oxidative stress biomarkers (malondialdehyde (MDA), total antioxidant capacity (TAC), and total oxidant status (TOS)) were measured. We demonstrated that treatment with NaHS ameliorated the impairment in the retrieval of reference memory and passive avoidance learning. Moreover, HFD increased anxiety-like behavior, which was reversed by the administration of NaHS. Additionally, the increase in MDA and TOS and the decrease in TAC induced by HFD in the serum and hippocampus were significantly reduced following administration of NaHS. These results indicate that NaHS could significantly ameliorate HFD-induced spatial and passive learning and memory impairment and anxiety-like behavior, at least in part, via its antioxidant activities. Therefore, the administration of NaHS can provide a therapeutic approach for HFD-induced memory impairment.
认知功能会因高脂肪饮食(HFD)的摄入增加而受损。此外,HFD 的摄入会改变硫化氢(HS)的代谢。HS 是一种具有抗氧化作用的重要信号分子,可调节大脑中的多种功能。在本研究中,我们研究了硫氢化钠(NaHS,HS 供体)对 HFD 摄入引起的认知障碍和氧化应激变化的影响。在 Wistar 大鼠进行 11 周的 HFD 饮食后,使用高架十字迷宫(EPM)、水迷宫(MWM)和被动回避学习(PAL)任务分别评估焦虑样行为以及空间和被动学习记忆。在饮食期间每天进行腹腔内注射 NaHS。测量血清和海马氧化应激生物标志物(丙二醛(MDA)、总抗氧化能力(TAC)和总氧化状态(TOS))。我们证明,NaHS 的治疗可改善参考记忆检索和被动回避学习的损伤。此外,HFD 增加了焦虑样行为,而 NaHS 的给药则逆转了这种行为。此外,NaHS 给药后,血清和海马中由 HFD 引起的 MDA 和 TOS 增加以及 TAC 减少显著减少。这些结果表明,NaHS 可以通过其抗氧化活性显著改善 HFD 诱导的空间和被动学习记忆损伤和焦虑样行为。因此,NaHS 的给药可以为 HFD 诱导的记忆损伤提供一种治疗方法。
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