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脑卒中GSK-3β调控内质网-线粒体偶联参与炎症性脑损伤的机制研究

雷建华 杜贺芳 刘昱肖

中风与神经疾病杂志2025,Vol.42Issue(7):637-640,4.
中风与神经疾病杂志2025,Vol.42Issue(7):637-640,4.DOI:10.19845/j.cnki.zfysjjbzz.2025.0122

脑卒中GSK-3β调控内质网-线粒体偶联参与炎症性脑损伤的机制研究

Mechanism of glycogen synthase kinase-3β participating in stroke-induced inflammatory brain injury by regulating endoplasmic reticulum-mitochondria coupling

雷建华 1杜贺芳 2刘昱肖2

作者信息

  • 1. 邯郸市中心医院神经内科,河北 邯郸 056000
  • 2. 华北医疗健康集团邢台总医院骨六科,河北 邢台 054000
  • 折叠

摘要

Abstract

Objective To investigate the mechanism of glycogen synthase kinase-3β(GSK-3β)participating in stroke-induced inflammatory brain injury through endoplasmic reticulum-mitochondria coupling,and to provide a theoreti-cal reference and potential targets for precise treatment.Methods A rat model of middle cerebral artery occlusion was es-tablished,and the rats were divided into sham-operation group,model group,and GSK-3β inhibitor(TDZD-8)intervention group.Neurological function score was used to evaluate the degree of brain injury;TTC staining was used to evaluate cere-bral infarct area;electron microscopy was used to observe mitochondrial ultrastructure;mitochondrial calcium concentra-tion was measured;ELISA was used to measure the levels of inflammatory factors[tumor necrosis factor-α(TNF-α)and in-terleukin-1β(IL-1β)],and Western blot was used to measure the expression levels of related proteins.Results Compared with the sham-operation group,the model group had significant neurological function impairment,an increase in cerebral infarct area,and significant increases in the expression levels of inflammatory factors and GSK-3β,with enhanced endoplas-mic reticulum-mitochondria coupling and mitochondrial calcium overload.TDZD-8 significantly improved the above indica-tors and reduced the levels of inflammatory factors and cerebral infarct area.Conclusion Abnormal activation of GSK-3β damages brain tissue by regulating endoplasmic reticulum-mitochondria coupling and promotes mitochondrial calcium over-load and inflammatory response.Inhibiting GSK-3β activity can effectively improve stroke-induced inflammatory brain in-jury,which provides a new pathway and a molecular target for developing precise treatment strategies.

关键词

脑卒中/糖原合成激酶-3β/内质网-线粒体偶联/脑损伤

Key words

Stroke/Glycogen synthase kinase-3β/Endoplasmic reticulum-mitochondria coupling/Brain injury

分类

医药卫生

引用本文复制引用

雷建华,杜贺芳,刘昱肖..脑卒中GSK-3β调控内质网-线粒体偶联参与炎症性脑损伤的机制研究[J].中风与神经疾病杂志,2025,42(7):637-640,4.

基金项目

2024河北省医学科学研究课题计划项目(20241660) (20241660)

中风与神经疾病杂志

1003-2754

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