生物学杂志

生物学杂志 ›› 2022, Vol. 39 ›› Issue (6): 14-.doi: 10.3969/j.issn.2095-1736.2022.06.014

• 研究报告 • 上一篇    下一篇

仙茅苷对抗PTSD诱导的小鼠海马炎症反应机制

  

  1. 安徽中医药大学新安医学教育部重点实验室， 合肥 230012
  • 出版日期:2022-12-18 发布日期:2022-12-12
  • 通讯作者: 朱国旗，博士，研究员，博士研究生导师，研究方向为神经精神疾病发病机理及中医药防治，E-mail: guoqizhu@gmail.com
  • 作者简介:姬曼曼，硕士研究生，研究方向为中药神经药理，E-mail: 1396055793@qq.com
  • 基金资助:
    国家自然科学基金项目（81673716）； 安徽省重点研发计划项目（202104j07020004）； 安徽省高等学校自然科研究项目（KJ2021A0575）

Mechanism of curculigoside against PTSD-induced inflammatory response in mouse hippocampus

  1. Key Laboratory of Xin’an Medicine, Ministry of Education, Anhui University of Chinese Medicine,
    Hefei 230012, China
  • Online:2022-12-18 Published:2022-12-12

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摘要： 仙茅苷（CUR）是仙茅的主要成分，具有多种生物活性。然而，CUR能否调控创伤后应激障碍（PTSD）诱导的小鼠海马炎症尚不清楚。采用改良的单次延长应激和电击（SPS&S）小鼠模型，探讨仙茅苷通过核转录因子κB（NF-κB）通路抑制PTSD小鼠海马神经炎症的作用机制。结果显示：与SPS&S模型组相比，仙茅苷能够显著降低PTSD小鼠在恐惧消退中的凝滞时间（P<0.05），增加其在旷场中心区域的运动时间与距离（P<0.05），并增加其在高架十字迷宫中进入开放臂的次数（P<0.05）；同时，仙茅苷能降低PTSD小鼠血清中促炎因子TNF-α与IL-1β的水平（P<0.05），改善其海马CA1区神经细胞的病理变化，降低其海马组织中NF-κB、NLRP3、Caspase-1的表达水平（P<0.05）。表明仙茅苷改善SPS&S诱导的PTSD小鼠焦虑样行为，可能是通过抑制NF-κB介导的神经炎症通路发挥作用。

关键词: 仙茅苷, 创伤后应激障碍, NF-κB, 炎症, 恐惧消退

Abstract: Curculigoside (CUR) is the main component of Curculigo and has various biological activities. However, it is not clear whether CUR inhibits post-traumatic stress disorder (PTSD)-induced inflammation in the hippocampus of mice. In this study, a modified mouse model of single prolonged stress and electrical stimulation (SPS&S) was established to investigate the effect of curculigoside on neuroinflammation in the hippocampus of SPS&S-treated mice from the prospective of nuclear factor kappa-B (NF-κB) pathway. The results showed that, compared with that of SPS&S group, CUR significantly reduced the freezing time of PTSD mice during fear extinction (P<0.05). It increased the movement time and distance in the central area in the open field test (P<0.05), and increased the number of open arms in the Elevated Plus Maze Test (P<0.05). In addition, compared with that of SPS&S group, CUR decreased the levels of TNF-α and IL-1β in serum of PTSD mice (P<0.05). It improved the pathological changes in CA1 regions of the hippocampus, and decreased hippocampal expressions of NF-κB, NLRP3, and Caspase-1(P<0.05). These data implicated that CUR improved PTSD-like behaviors in mice, which might be related to the regulation of NF-κB-dependent neuroinflammation.

Key words: curculigoside, post-traumatic stress disorder, NF-κB, inflammation, fear extinction

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