摘要
目的探讨补体C3及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。方法将90只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+补体C3抑制剂组。用Y迷宫试验检测工作记忆,用q RT-PCR法检测C1q和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和C3 mRNA及TGFβ1和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和C3 mRNA及TGFβ1和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。
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.
作者
郄晓娟
李清开
刘颖
冯雪妍
霍修林
张秀宁
霍佳
李志华
于海磊
徐贯杰
QIE Xiaojuan;LI Qingkai;LIU Ying;FENG Xueyan;HUO Xiulin;ZHANG Xiuning;HUO Jia;LI Zhihua;YU Hailei;XU Guanjie(Depart-ment of Anesthesiology,the Third Hospital of Hebei Medical University,Shijiazhuang 050051,China;不详)
出处
《实用医学杂志》
CAS
北大核心
2023年第2期204-208,共5页
The Journal of Practical Medicine
基金
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)。
