基于血清代谢组学和生物网络分析研究CD-1退役种鼠攻击行为的生物学机制
CSTR:
作者:
作者单位:

山西大学中医药现代研究中心,山西大学地产中药功效物质研究与利用山西省重点实验室 太原 030006

作者简介:

胡婷,女,硕士研究生;研究方向:中药药理作用机制;E-mail:ht19990529@126.com。

通讯作者:

中图分类号:

Q955

基金项目:

国家自然科学基金项目(No. 82374153);


Serum Metabolomics and Bio-Network Analysis Reveal the Biological Mechanism of Aggressive Behavior in CD-1 Retired Breeder Mice
Author:
Affiliation:

Modern Research Center for Traditional Chinese Medicine, Shanxi Key Laboratory of Active Constituents Research and Utilization of TCM, Shanxi University, Taiyuan 030006, China

Fund Project:

  • 摘要
  • |
  • 图/表
  • |
  • 访问统计
  • |
  • 参考文献
  • |
  • 相似文献
  • |
  • 引证文献
  • |
  • 资源附件
  • |
  • 文章评论
    摘要:

    本文旨在研究CD-1退役种鼠攻击行为发生过程中涉及到的代谢途径及相关基因,阐明其攻击行为发生的生物学机制,为慢性社交挫败应激抑郁模型的科学研究和规范操作提供依据。在慢性社交挫败应激抑郁模型攻击小鼠筛选阶段,首先将CD-1退役种鼠单笼饲养一周,培养其领地意识,然后通过驻地入侵实验分别筛选出对入侵者具有攻击性(攻击组)以及不具有攻击性(非攻击组)的小鼠。采用超高效液相色谱-串联质谱代谢组学技术寻找攻击组小鼠和非攻击组小鼠之间的差异代谢物和代谢途径;并整合生物网络分析挖掘小鼠攻击行为发生的关键代谢途径及关键基因。结果显示,攻击组小鼠和非攻击组小鼠血清中共有12种差异代谢物,包括胆碱、1-酰基-sn-甘油-3-磷酸胆碱、甘油磷酰乙醇胺、油酸酰胺、反式-棕榈油酸、DL-谷氨酸、亚油酰胺、硬脂酸、N-乙酰-L-亮氨酸、肉毒碱、胆酸和脱氢抗坏血酸。同时,综合生物网络分析结果,发现甘油磷脂代谢可能是攻击行为发生的关键通路,Pld1、Pld2、Pla2g5、Pla2g3、Pla2g10、Lypla1、LcatChkaChat这9个基因可能是攻击行为与差异代谢物交集基因中的关键基因。因此,推测CD-1退役种鼠攻击行为的发生主要由甘油磷脂代谢途径中关键基因的变化引起。

    Abstract:

    [Objectives] Aggressive behavior represents a prevalent manifestation of mental disorders, with severe violence posing detrimental consequences for the society. During the screening of CD-1 retired breeder mice, we found significant differences in aggression among individuals, and selecting those with higher aggression is crucial for successfully establishing the model of depression induced by chronic social defeat stress (CSDS). Therefore, this study investigates the metabolic pathways and related genes in CD-1 retired breeder mice during aggressive behavior, aiming to reveal the mechanisms of aggressive behavior. [Methods] During the screening phase of aggressive mice of the CSDS-induced depression model, CD-1 retired breeder mice were housed in individual cages for a week to establish territorial awareness, and then attack and non-attack mice were screened out through the resident-intruder test. Compound Discoverer 3.0 was used for serum metabolomics based on ultra performance liquid chromatography-tandem mass spectrometry to identify differential metabolites and metabolic pathways between the attack group and the non-attack group of mice. Meanwhile, biological network analysis based on Cytoscape 3.9.1 software was performed to identify key metabolic pathways and genes involved in the occurrence of aggressive behavior. Independent samples t-test was performed to compare the aggressive behavior between the two groups. [Results] The serum metabolomics (Appendix 1) screened out 12 differential metabolites between the attack group and non-attack group of CD-1 retired breeder mice. Among them, DL-glutamic acid, N-acetyl-L-leucine, dehydroascorbic acid, oleamide, trans-palmitoleate, choline, and linoleamide were significantly increased, while tetradecanoylcarnitine, cholic acid, 1-acyl-sn-glycero-3-phosphocholine, sn-glycero-3-phosphoethanolamine, and octadecanoic acid were significantly decreased (P < 0.05). The results above, combined with those of biological network analysis (Figs. 5, 6 and Table 3), show that glycerophospholipid metabolism is a key pathway for aggressive behavior and Pld1, Pld2, Pla2g5, Pla2g3, Pla2g10, Lypla1, Lcat, Chka, and Chat in the metabolic pathway may be key genes shared by aggressive behavior and differential metabolites (Table 4). [Conclusion] The occurrence of aggressive behavior may be closely related to glycerophospholipid metabolism, which is not only significant for elucidating the metabolome of aggressive behavior in CD-1 retired breeder mice but also of great value for the scientific research and standardization of the model of CSDS-induced depression.

    参考文献
    相似文献
    引证文献
引用本文

胡婷,王琦,赵云昊,李凯文,王育静,秦雪梅,田俊生. 2025.基于血清代谢组学和生物网络分析研究CD-1退役种鼠攻击行为的生物学机制. 动物学杂志, 60(5): 702-719.

复制
分享
相关视频

文章指标
  • 点击次数:
  • 下载次数:
  • HTML阅读次数:
  • 引用次数:
历史
  • 收稿日期:2024-11-22
  • 最后修改日期:
  • 录用日期:
  • 在线发布日期: 2025-10-21
  • 出版日期:
文章二维码