Xiang Zhou, Peiyi Yang, Chaonan Dong, Huimin Chang, Fan Zhang, Qi Shu, Naixuan Wei, Bin Zhang, Yan Wu, Wenjing Shao, Ronglin Cai, Qing Yu
{"title":"电针预处理通过抑制下丘脑外侧小胶质细胞吞噬减轻心肌缺血再灌注损伤","authors":"Xiang Zhou, Peiyi Yang, Chaonan Dong, Huimin Chang, Fan Zhang, Qi Shu, Naixuan Wei, Bin Zhang, Yan Wu, Wenjing Shao, Ronglin Cai, Qing Yu","doi":"10.1111/cns.70595","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Aim</h3>\n \n <p>The occurrence of myocardial ischemia–reperfusion injury (MIRI) is accompanied by neuroinflammatory reactions and is closely related to the overactivation of microglia. Currently, effective clinical strategies to prevent MIRI are unclear. This study investigated potential therapeutic targets and the mechanisms of electroacupuncture pretreatment (EA-pre) for MIRI.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>A MIRI mouse model was established by ligating the left anterior descending branch of the heart for 30 min and reperfusion for 2 h. The mechanisms by which EA-pre alleviates MIRI were investigated through immunofluorescence staining, chemogenetics, and fiber photometry recordings, focusing on the potential involvement of microglia and glutamate (Glu) neurons in the lateral hypothalamic (LH).</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>EA-pre improves cardiac function in MIRI mice by suppressing microglial activation in the LH. The underlying mechanism likely involves EA-pre inhibition of microglial engulfment of inhibitory synapses around LH<sup>Glu</sup> neurons. Targeted activation of LH<sup>microglia</sup> reverses EA's inhibitory effect, thereby increasing LH<sup>Glu</sup> neuronal activity and triggering overactivation of the sympathetic nervous system (SNS), which ultimately exacerbates MIRI.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>EA-pre inhibits microglial engulfment of inhibitory synapses around LH<sup>Glu</sup> neurons in MIRI mice, thereby suppressing LH<sup>Glu</sup> neuronal activity, reducing SNS output, and ultimately exerting cardioprotective effects.</p>\n </section>\n </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"31 9","pages":""},"PeriodicalIF":5.0000,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cns.70595","citationCount":"0","resultStr":"{\"title\":\"Electroacupuncture Pretreatment Alleviates Myocardial Ischemia–Reperfusion Injury by Inhibiting Engulfment by Microglia in the Lateral Hypothalamus\",\"authors\":\"Xiang Zhou, Peiyi Yang, Chaonan Dong, Huimin Chang, Fan Zhang, Qi Shu, Naixuan Wei, Bin Zhang, Yan Wu, Wenjing Shao, Ronglin Cai, Qing Yu\",\"doi\":\"10.1111/cns.70595\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Aim</h3>\\n \\n <p>The occurrence of myocardial ischemia–reperfusion injury (MIRI) is accompanied by neuroinflammatory reactions and is closely related to the overactivation of microglia. Currently, effective clinical strategies to prevent MIRI are unclear. This study investigated potential therapeutic targets and the mechanisms of electroacupuncture pretreatment (EA-pre) for MIRI.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Methods</h3>\\n \\n <p>A MIRI mouse model was established by ligating the left anterior descending branch of the heart for 30 min and reperfusion for 2 h. The mechanisms by which EA-pre alleviates MIRI were investigated through immunofluorescence staining, chemogenetics, and fiber photometry recordings, focusing on the potential involvement of microglia and glutamate (Glu) neurons in the lateral hypothalamic (LH).</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>EA-pre improves cardiac function in MIRI mice by suppressing microglial activation in the LH. The underlying mechanism likely involves EA-pre inhibition of microglial engulfment of inhibitory synapses around LH<sup>Glu</sup> neurons. 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Electroacupuncture Pretreatment Alleviates Myocardial Ischemia–Reperfusion Injury by Inhibiting Engulfment by Microglia in the Lateral Hypothalamus
Aim
The occurrence of myocardial ischemia–reperfusion injury (MIRI) is accompanied by neuroinflammatory reactions and is closely related to the overactivation of microglia. Currently, effective clinical strategies to prevent MIRI are unclear. This study investigated potential therapeutic targets and the mechanisms of electroacupuncture pretreatment (EA-pre) for MIRI.
Methods
A MIRI mouse model was established by ligating the left anterior descending branch of the heart for 30 min and reperfusion for 2 h. The mechanisms by which EA-pre alleviates MIRI were investigated through immunofluorescence staining, chemogenetics, and fiber photometry recordings, focusing on the potential involvement of microglia and glutamate (Glu) neurons in the lateral hypothalamic (LH).
Results
EA-pre improves cardiac function in MIRI mice by suppressing microglial activation in the LH. The underlying mechanism likely involves EA-pre inhibition of microglial engulfment of inhibitory synapses around LHGlu neurons. Targeted activation of LHmicroglia reverses EA's inhibitory effect, thereby increasing LHGlu neuronal activity and triggering overactivation of the sympathetic nervous system (SNS), which ultimately exacerbates MIRI.
Conclusion
EA-pre inhibits microglial engulfment of inhibitory synapses around LHGlu neurons in MIRI mice, thereby suppressing LHGlu neuronal activity, reducing SNS output, and ultimately exerting cardioprotective effects.
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.
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