生物学杂志

生物学杂志 ›› 2026, Vol. 43 ›› Issue (2): 77-.doi: 10.3969/j.issn.2095-1736.2026.02.077

• 研究报告 • 上一篇    下一篇

G1通过修复海马神经元及星形胶质细胞损伤改善小鼠PTSD样行为

牛静雯1， 杨绍杰2， 朱国旗1， 陈丽霞1   

  1. 1. 安徽中医药大学分子生物学（脑病）重点实验室， 合肥 230012；
    2. 安徽中医药大学第二附属医院， 合肥 230061
  • 出版日期:2026-04-18 发布日期:2026-04-23
  • 通讯作者: 朱国旗，博士，研究员，研究方向为中药神经药理学，E-mail：guoqizhu@gmail.com；陈丽霞，硕士，助理实验师，研究方向为中药神经药理学，E-mail：c994743@163.com；朱国旗和陈丽霞为共同通信作者
  • 作者简介:牛静雯，硕士研究生，研究方向为神经药理学，E-mail：2820767247@qq.com
  • 基金资助:
    国家自然科学基金项目（82404890）； 安徽省高等学校科学研究项目（2024AH040137， 2024AH051044）； 中医药防治神志病团队项目（2024zyky02）； 国家中医药管理局中医基础理论高水平重点学科开放课题（ZYJCLLZD-04）

G1 ameliorates PTSD-like behaviors in mice by repairing damage to hippocampal neurons and astrocytes

NIU Jingwen1, YANG Shaojie2, ZHU Guoqi1, CHEN Lixia1   

  1. 1. Key Laboratory of Molecular Biology （Brain Diseases）, Anhui University of Chinese Medicine, Hefei 230012, China;
    2. The Second Affiliation Hospital of Anhui University of Chinese Medicine, Hefei 230061, China
  • Online:2026-04-18 Published:2026-04-23

摘要： G1是G蛋白偶联受体30（G protein-coupled estrogen receptor 30, GPR30）的特异性激动剂，但其能否修复创伤后应激障碍（post-traumatic stress disorder, PTSD）引起的海马神经元与星形胶质细胞损伤尚不清楚。本研究通过单一长时程应激（single prolonged stress, SPS）建立PTSD模型小鼠，旨在探讨G1对SPS模型小鼠PTSD样行为的影响，并基于海马神经元和星形胶质细胞的变化分析其潜在机制。结果显示，SPS模型组小鼠表现出明显的焦虑、抑郁及恐惧记忆消退困难等PTSD样行为（P＜0.05），同时海马内GPR30、胶质纤维酸性蛋白（glial fibrillary acidic protein, GFAP）及连接蛋白43（connexin 43, Cx43）表达下调。经G1干预后，PTSD样行为显著改善（P＜0.05），GPR30、GFAP和Cx43表达上调，海马变性神经元数量也明显减少。结果表明，G1能够改善SPS诱导的小鼠PTSD样行为，其机制可能与修复海马神经元及星形胶质细胞损伤有关。

关键词: 创伤后应激障碍, G蛋白偶联受体30, 神经元, 星形胶质细胞

Abstract: G1 is a specific agonist of G protein-coupled estrogen receptor 30 (GPR30). However, it remains unclear whether G1 can repair the damage to hippocampal neurons and astrocytes induced by post-traumatic stress disorder (PTSD). To investigate the effects of G1 on PTSD-like behaviors and its underlying mechanisms, a PTSD mouse model was established using the single prolonged stress (SPS) method and analyzed subsequent changes in hippocampal neurons and astrocytes. The results showed that mice in the SPS model group exhibited significant PTSD-like behaviors, including anxiety, depression, and impaired fear extinction (P<0.05). Concurrently, the expressions of GPR30, glial fibrillary acidic protein (GFAP), and connexin 43 (Cx43) in the hippocampus were downregulated. Following G1 intervention, PTSD-like behaviors were significantly ameliorated (P<0.05). The expressions of GPR30, GFAP, and Cx43 were upregulated, and the number of degenerated neurons in the hippocampus was notably reduced. These findings suggest that G1 improves PTSD-like behaviors in SPS mice, and its therapeutic mechanism may be associated with the repair of hippocampal neuronal and astrocyte damage.

Key words: post-traumatic stress disorder, G protein-coupled receptor 30, neuron, astrocyte

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