实用医学杂志 ›› 2023, Vol. 39 ›› Issue (2): 204-208.doi: 10.3969/j.issn.1006⁃5725.2023.02.014

• 基础研究 • 上一篇    下一篇

基于补体C3及TGFβ1/Smad信号通路探究七氟烷麻醉对老龄小鼠突触可塑性及工作记忆力损伤的机制

郄晓娟1 李清开1 刘颖1 冯雪妍1 霍修林1 张秀宁1 霍佳2 李志华1 于海磊3 徐贯杰1   

  1. 河北医科大学第三医院1 麻醉科,2 骨病科(石家庄050051);3 河北医科大学法医学院(石家庄050011)
  • 出版日期:2023-01-25 发布日期:2023-01-25
  • 通讯作者: 徐贯杰 E⁃mail:xgj658950@126.com
  • 基金资助:
    河北省自然科学基金面上项目(编号:H2019206609);河北省医学科学研究课题(编号:20220125)

Based on complement C3 and TGFβ1/Smad signal pathway to explore the mechanism of sevoflurane anes⁃ thesia on synaptic plasticity and working memory impairment in aged mice 

QIE Xiaojuan*,LI Qingkai, LIU Ying,FENG Xueyan,HUO Xiulin,ZHANG Xiuning,HUO Jia,LI Zhihua,YU Hailei,XU Guanjie.   

  1. Depart⁃ ment of Anesthesiologythe Third Hospital of Hebei Medical UniversityShijiazhuang 050051China 
  • Online:2023-01-25 Published:2023-01-25
  • Contact: XU Guanjie E⁃mail:xgj658950@126.com

摘要:

目的 探讨补体 C3 TGFβ1/Smad 信号通路在七氟烷麻醉对老龄小鼠突触可塑性及工作记 忆力损伤中的作用。方法  90 C57BL/6 小鼠随机分为 3 组,对照组、七氟烷麻醉组和七氟烷麻醉+ C3 抑制剂组。用 Y 迷宫试验检测工作记忆,用 qRT⁃PCR 法检测 C1q C3 mRNA 表达;用长时程增强效 应(LTP)评价突触可塑性,用 Western blot 法检测 TGFβ1/Smad3 通路蛋白表达。结果 七氟烷麻醉抑制小 鼠自发交替率和 LTP 实验的群峰电位(PS)增幅,促进 C1q C3 mRNA TGFβ1 Smad3 蛋白表达;补 体分子 C3 抑制剂促进小鼠自发交替率和 PS 增幅,抑制 C1q C3 mRNA TGFβ1 Smad3 蛋白表达。 结论 七氟烷麻醉可导致老龄小鼠工作记忆水平和突触可塑性下降,其机制可能与补体 C3 介导 TGFβ1/ smad 信号通路有关。

关键词:

补体C3, TGFβ1, Smad3, 麻醉药, 吸入, 老年人, 海马, 认知

Abstract:

Objective To investigate the effect of complement C3 and TGFβ1/Smad signal pathway on synaptic plasticity and working memory impairment in sevoflurane ⁃ anesthetiezd elderly mice. Methods Ninety C57BL/6 mice were randomly divided into three groups including a control group,sevoflurane anesthesia group and sevoflurane anesthesia plus complement C3 inhibitor group. Working memory was detected by Y⁃maze test and the mRNA expressions of C1q and C3 were detected by RT⁃PCR. Synaptic plasticity was assessed by long⁃term potentiation(LTP),and protein expression of the TGFβ1/Smad3 pathway was detected by Western blot. Results Sevoflurane anesthesia inhibited spontaneous alternation and decreased population spike(PS)amplitude in LTP. The mRNA expressions of C1q and C3 were increased,so were the protein expressions of TGFβ1 and Smad3. Complement molecule C3 inhibitors enhanced both spontaneous alternation and PS amplitude,while suppressed the mRNA expressions of C1q and C3 and the protein expressions of TGFβ1 and Smad3. Conclusions Sevoflurane anesthesia leads to a decline in working memory and synaptic plasticity in elderly mice,possibly through regulating the complement C3⁃mediated TGFβ1/smad signal pathway. 

Key words:

complement C3, TGFβ1, Smad3, anesthetics, inhalation, aged, hippocampus, cognition