{"title":"Electroacupuncture attenuates middle cerebral artery occlusion-induced learning and memory impairment by regulating microglial polarization in hippocampus.","authors":"Qiong Wen, Fubing Zha, Linlin Shan, Shaohua Zhang, Peng Xiao, Chunxia Zhang, Haibo Yu, Yulong Wang","doi":"10.1080/00207454.2024.2313664","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>As a traditional medical therapy, electroacupuncture (EA) has been demonstrated to have beneficial effects on ischemic stroke-induced cognitive impairment. However, the underlying mechanism is largely unclear.</p><p><strong>Methods: </strong>Adult rats received occlusion of the middle cerebral artery and reperfusion (MCAO/R) to establish the ischemic stroke model. Morris water maze test was performed following EA stimulation at the GV20, PC6, and KI1 acupoints in rats to test the learning and memory ability. Western blot, immunofluorescent staining, and enzyme-linked immunosorbent assay were conducted to assess the cellular and molecular mechanisms.</p><p><strong>Results: </strong>EA stimulation attenuated neurological deficits. In the Morris water maze test, EA treatment ameliorated the MCAO/R-induced learning and memory impairment. Moreover, we observed that MCAO/R induced microglial activation and polarization in the ischemic hippocampus, whereas, EA treatment dampened microglial activation and inhibited M1 microglial polarization but enhanced M2 microglial polarization. EA treatment inhibited the increased expression of proinflammatory cytokines and enhanced the increased expression of anti-inflammatory cytokines. Finally, we found that EA treatment dampened microglial p38 mitogen-activated protein kinase (MAPK) phosphorylation.</p><p><strong>Conclusion: </strong>Collectively, our data suggested that EA treatment ameliorated cognitive impairment induced by MCAO/R and the underlying mechanism may be <i>p</i>38-mediated microglia polarization and neuroinflammation.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"626-638"},"PeriodicalIF":1.5000,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Neuroscience","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/00207454.2024.2313664","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/2/14 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Background: As a traditional medical therapy, electroacupuncture (EA) has been demonstrated to have beneficial effects on ischemic stroke-induced cognitive impairment. However, the underlying mechanism is largely unclear.
Methods: Adult rats received occlusion of the middle cerebral artery and reperfusion (MCAO/R) to establish the ischemic stroke model. Morris water maze test was performed following EA stimulation at the GV20, PC6, and KI1 acupoints in rats to test the learning and memory ability. Western blot, immunofluorescent staining, and enzyme-linked immunosorbent assay were conducted to assess the cellular and molecular mechanisms.
Results: EA stimulation attenuated neurological deficits. In the Morris water maze test, EA treatment ameliorated the MCAO/R-induced learning and memory impairment. Moreover, we observed that MCAO/R induced microglial activation and polarization in the ischemic hippocampus, whereas, EA treatment dampened microglial activation and inhibited M1 microglial polarization but enhanced M2 microglial polarization. EA treatment inhibited the increased expression of proinflammatory cytokines and enhanced the increased expression of anti-inflammatory cytokines. Finally, we found that EA treatment dampened microglial p38 mitogen-activated protein kinase (MAPK) phosphorylation.
Conclusion: Collectively, our data suggested that EA treatment ameliorated cognitive impairment induced by MCAO/R and the underlying mechanism may be p38-mediated microglia polarization and neuroinflammation.
背景:作为一种传统医学疗法,电针(EA)已被证实对缺血性脑卒中引起的认知功能障碍有益处。然而,其基本机制尚不清楚:方法:成年大鼠接受大脑中动脉闭塞再灌注(MCAO/R)治疗,建立缺血性中风模型。方法:成年大鼠接受大脑中动脉闭塞再灌注(MCAO/R)治疗后,在GV20、PC6和KI1穴位进行EA刺激,进行莫里斯水迷宫测试,以检测大鼠的学习和记忆能力。研究还采用了 Western 印迹、免疫荧光染色和酶联免疫吸附试验来评估细胞和分子机制:结果:EA刺激减轻了神经系统缺陷。在莫里斯水迷宫测试中,EA治疗可改善MCAO/R诱导的学习和记忆障碍。此外,我们还观察到,MCAO/R诱导缺血海马的小胶质细胞活化和极化,而EA治疗抑制了小胶质细胞的活化,抑制了M1小胶质细胞的极化,但增强了M2小胶质细胞的极化。EA 治疗抑制了促炎细胞因子表达的增加,增强了抗炎细胞因子表达的增加。最后,我们发现 EA 治疗抑制了小胶质细胞 p38 丝裂原活化蛋白激酶(MAPK)磷酸化:总之,我们的数据表明,EA治疗可改善MCAO/R诱导的认知障碍,其潜在机制可能是p38介导的小胶质细胞极化和神经炎症。
期刊介绍:
The International Journal of Neuroscience publishes original research articles, reviews, brief scientific reports, case studies, letters to the editor and book reviews concerned with problems of the nervous system and related clinical studies, epidemiology, neuropathology, medical and surgical treatment options and outcomes, neuropsychology and other topics related to the research and care of persons with neurologic disorders. The focus of the journal is clinical and transitional research. Topics covered include but are not limited to: ALS, ataxia, autism, brain tumors, child neurology, demyelinating diseases, epilepsy, genetics, headache, lysosomal storage disease, mitochondrial dysfunction, movement disorders, multiple sclerosis, myopathy, neurodegenerative diseases, neuromuscular disorders, neuropharmacology, neuropsychiatry, neuropsychology, pain, sleep disorders, stroke, and other areas related to the neurosciences.