Electroacupuncture Improves Microglial Polarization Induced-Inflammation by Regulating the TGF-β/Smad-3 Signaling Pathway in Ischemic Stroke Mice

IF 5 1区医学 Q1 NEUROSCIENCES

CNS Neuroscience & Therapeutics Pub Date : 2025-08-20 DOI:10.1111/cns.70567

Guoqiang Yang, Liulu Zhang, Yanlin Yuan, Maryam Mazhar, Dechou Zhang, Yong Liu, Guiquan Chen, Xuehui Fan

{"title":"Electroacupuncture Improves Microglial Polarization Induced-Inflammation by Regulating the TGF-β/Smad-3 Signaling Pathway in Ischemic Stroke Mice","authors":"Guoqiang Yang, Liulu Zhang, Yanlin Yuan, Maryam Mazhar, Dechou Zhang, Yong Liu, Guiquan Chen, Xuehui Fan","doi":"10.1111/cns.70567","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Aims</h3>\n \n <p>This study aimed to investigate the mechanisms underlying the therapeutic effects of electroacupuncture (EA) at the Dazhui (GV14) and Baihui (GV20) acupoints in the treatment of ischemic stroke (IS).</p>\n </section>\n \n <section>\n \n <h3> Methods and Results</h3>\n \n <p>The therapeutic efficacy of EA was evaluated using a middle cerebral artery occlusion (MCAO) mouse model. Neurological function was assessed through behavioral assessments, and infarct volume was measured using magnetic resonance imaging. Techniques such as immunofluorescence and western blotting were employed to analyze neural injury recovery, neuroinflammation, microglia/macrophage activation and polarization, as well as alterations in the TGF-β/Smad3 signaling pathway. Our findings demonstrated that EA significantly improved neurological function and reduced infarct volume in MCAO mice. Furthermore, EA attenuated neuroinflammation by suppressing the polarization of microglia toward the pro-inflammatory M1 phenotype. Additionally, EA decreased the expression of TGF-β and Smad3 proteins following MCAO.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>EA may inhibit the M1 polarization of microglia/macrophages and provide a protective effect against ischemic brain injury by modulating the TGF-β/Smad-3 signaling pathway. These findings suggest that EA could be a potential therapeutic strategy for IS treatment.</p>\n </section>\n </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"31 8","pages":""},"PeriodicalIF":5.0000,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cns.70567","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"CNS Neuroscience & Therapeutics","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/cns.70567","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"NEUROSCIENCES","Score":null,"Total":0}

引用次数: 0

Abstract

Aims

This study aimed to investigate the mechanisms underlying the therapeutic effects of electroacupuncture (EA) at the Dazhui (GV14) and Baihui (GV20) acupoints in the treatment of ischemic stroke (IS).

Methods and Results

The therapeutic efficacy of EA was evaluated using a middle cerebral artery occlusion (MCAO) mouse model. Neurological function was assessed through behavioral assessments, and infarct volume was measured using magnetic resonance imaging. Techniques such as immunofluorescence and western blotting were employed to analyze neural injury recovery, neuroinflammation, microglia/macrophage activation and polarization, as well as alterations in the TGF-β/Smad3 signaling pathway. Our findings demonstrated that EA significantly improved neurological function and reduced infarct volume in MCAO mice. Furthermore, EA attenuated neuroinflammation by suppressing the polarization of microglia toward the pro-inflammatory M1 phenotype. Additionally, EA decreased the expression of TGF-β and Smad3 proteins following MCAO.

Conclusion

EA may inhibit the M1 polarization of microglia/macrophages and provide a protective effect against ischemic brain injury by modulating the TGF-β/Smad-3 signaling pathway. These findings suggest that EA could be a potential therapeutic strategy for IS treatment.

Abstract Image

查看原文本刊更多论文

电针通过调节TGF-β/Smad-3信号通路改善缺血性脑卒中小鼠小胶质细胞极化诱导的炎症

目的探讨电针大椎（GV14）和百会（GV20）穴治疗缺血性脑卒中（IS）的作用机制。方法与结果采用小鼠大脑中动脉闭塞（MCAO）模型评价EA的治疗效果。通过行为评估评估神经功能，并使用磁共振成像测量梗死体积。采用免疫荧光和western blotting等技术分析神经损伤恢复、神经炎症、小胶质细胞/巨噬细胞活化和极化以及TGF-β/Smad3信号通路的变化。我们的研究结果表明，EA可显著改善MCAO小鼠的神经功能并减少梗死体积。此外，EA通过抑制小胶质细胞向促炎M1表型的极化来减轻神经炎症。此外，EA可降低MCAO后TGF-β和Smad3蛋白的表达。结论EA可能通过调节TGF-β/Smad-3信号通路，抑制小胶质细胞/巨噬细胞M1极化，对缺血性脑损伤具有保护作用。这些发现表明EA可能是IS治疗的潜在治疗策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

CNS Neuroscience & Therapeutics 医学-神经科学

CiteScore

7.30

自引率

12.70%

发文量

240

审稿时长

2 months

期刊介绍： CNS Neuroscience & Therapeutics provides a medium for rapid publication of original clinical, experimental, and translational research papers, timely reviews and reports of novel findings of therapeutic relevance to the central nervous system, as well as papers related to clinical pharmacology, drug development and novel methodologies for drug evaluation. The journal focuses on neurological and psychiatric diseases such as stroke, Parkinson’s disease, Alzheimer’s disease, depression, schizophrenia, epilepsy, and drug abuse.