| 注册
首页|期刊导航|河北医学|重复经颅磁联合高压氧通过调控AKT/GSK3β/β-catenin通路改善迟发性脑病神经功能

重复经颅磁联合高压氧通过调控AKT/GSK3β/β-catenin通路改善迟发性脑病神经功能

戈蕾 李姣 王晓娜 于丽娜 王欢欢 武婧月

河北医学2026,Vol.32Issue(3):421-429,9.
河北医学2026,Vol.32Issue(3):421-429,9.DOI:10.3969/j.issn.1006-6233.2026.03.011

重复经颅磁联合高压氧通过调控AKT/GSK3β/β-catenin通路改善迟发性脑病神经功能

Repetitive Transcranial Magnetic Stimulation Combined with Hyperbaric Oxygen Therapy Improving Neurological Function in Delayed Encephalopathy by Modulating the AKT/GSK3β/β-Catenin Pathway

戈蕾 1李姣 1王晓娜 1于丽娜 1王欢欢 1武婧月1

作者信息

  • 1. 河北北方学院附属第一医院,河北 张家口 075000
  • 折叠

摘要

Abstract

Objective:To investigate the effects of repetitive transcranial magnetic stimulation(rTMS)combined with hyperbaric oxygen(HBO)on neurological function in rats with delayed encephalopathy after a-cute carbon monoxide poisoning(DEACMP)and to explore the underlying mechanism based on the AKT/GSK3β/β-catenin signaling pathway.Methods:Wistar rats with qualified cognitive function,as screened by the Morris water maze test,were randomly divided into six groups(n=10 per group):Ctrl group,DEACMP model group,HBO group,rTMS group,rTMS+HBO combination group,and MK-2206 group(rTMS+HBO+AKT inhibitor MK-2206).The DEACMP model was established using a static carbon monoxide inhalation method.The Morris water maze test was employed to assess cognitive behavioral performance.Histological staining was used to observe pathological changes in hippocampal neurons.Serum levels of oxidative stress markers(ROS,MDA,SOD),inflammatory factors(IL-6,IL-18),and myelin basic protein(MBP)were measured by ELISA.Neuronal apoptosis was detected by TUNEL staining.The expression levels of apoptosis-related proteins(Bax,Bcl-2,CytC,Caspase-3)and key proteins in the AKT/GSK3β/β-catenin pathway(p-AKT/AKT,p-GSK3β Ser9/GSK3β Ser9,nuclear β-catenin)were determined by Western blotting.Re-sults:Compared with the Ctrl group,the escape latency,ROS and MDA levels,IL-6,IL-18 and MBP lev-els,neuronal apoptosis rate,Bax,CytC and Caspase-3 expression levels were significantly increased in the DEACMP group(P<0.05).The number of crossing the platform,SOD level,Bcl-2,p-AKT/AKT,p-GSK3βSer9/GSK3βSer9 and nuclear β-catenin expression levels were significantly decreased(P<0.05).Compared with DEACMP group,the escape latency,ROS and MDA levels,IL-6,IL-18 and MBP levels,neuronal apoptosis rate,Bax,CytC and Caspase-3 expression levels in HBO group and rTMS group were sig-nificantly decreased(P<0.05).The number of crossing the platform,SOD level,Bcl-2,p-AKT/AKT,p-GSK3β Ser9/GSK3β Ser9 and nuclear β-catenin expression levels were significantly increased(P<0.05).Compared with HBO group and rTMS group,the escape latency,ROS and MDA levels,IL-6,IL-18 and MBP levels,neuronal apoptosis rate,Bax,CytC and Caspase-3 expression levels in rTMS+HBO group were significantly decreased(P<0.05).The number of crossing the platform,SOD level,Bcl-2,p-AKT/AKT,p-GSK3β Ser9/GSK3β Ser9 and nuclear β-catenin expression levels were significantly increased(P<0.05).Compared with the rTMS+HBO group,the escape latency,ROS and MDA levels,IL-6,IL-18 and MBP lev-els,neuronal apoptosis rate,Bax,CytC and Caspase-3 expression levels were significantly increased in the MK-2206 group(P<0.05).The number of crossing the platform,SOD level,Bcl-2,p-AKT/AKT,p-GSK3β Ser9/GSK3β Ser9 and nuclear β-caten in expression levels were significantly decreased(P<0.05).Conclusion:The combination of rTMS and HBO exerts a significant neuroprotective effect against DEACMP.The mechanism is likely associated with the synergistic activation of the AKT/GSK3β/β-catenin signaling pathway,leading to the integrated suppression of oxidative stress,inflammatory response,and neuronal apop-tosis.

关键词

一氧化碳中毒迟发性脑病/重复经颅磁/高压氧/神经功能/MBP/AKT/GSK3β/β-catenin

Key words

Delayed encephalopathy after carbon monoxide poisoning/Repetitive transcranial mag-netic stimulation/Hyperbaric oxygen/Neurological function/MBP/AKT/GSK3β/β-catenin

引用本文复制引用

戈蕾,李姣,王晓娜,于丽娜,王欢欢,武婧月..重复经颅磁联合高压氧通过调控AKT/GSK3β/β-catenin通路改善迟发性脑病神经功能[J].河北医学,2026,32(3):421-429,9.

基金项目

河北省医学科学研究课题计划资助,(编号:20241008) (编号:20241008)

河北医学

1006-6233

访问量0
|
下载量0
段落导航相关论文