Electroacupuncture Pretreatment Alleviates Myocardial Ischemia–Reperfusion Injury by Inhibiting Engulfment by Microglia in the Lateral Hypothalamus

IF 5 1区医学 Q1 NEUROSCIENCES

CNS Neuroscience & Therapeutics Pub Date : 2025-09-04 DOI:10.1111/cns.70595

Xiang Zhou, Peiyi Yang, Chaonan Dong, Huimin Chang, Fan Zhang, Qi Shu, Naixuan Wei, Bin Zhang, Yan Wu, Wenjing Shao, Ronglin Cai, Qing Yu

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Abstract

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 LH^Glu neurons. Targeted activation of LH^microglia reverses EA's inhibitory effect, thereby increasing LH^Glu 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 LH^Glu neurons in MIRI mice, thereby suppressing LH^Glu neuronal activity, reducing SNS output, and ultimately exerting cardioprotective effects.

Abstract Image

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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

目的心肌缺血再灌注损伤（MIRI）的发生伴有神经炎症反应，与小胶质细胞过度活化密切相关。目前，预防MIRI的有效临床策略尚不清楚。本研究探讨电针预处理（EA-pre）治疗MIRI的潜在靶点及机制。方法结扎左前降支30min，再灌注2h，建立小鼠MIRI模型。通过免疫荧光染色、化学遗传学和纤维光度法记录，研究了ea预缓解MIRI的机制，重点研究了小胶质细胞和谷氨酸（Glu）神经元在下丘脑外侧（LH）的潜在参与。结果EA-pre通过抑制LH小胶质细胞活化改善MIRI小鼠心功能。潜在的机制可能涉及ea预抑制小胶质吞噬LHGlu神经元周围的抑制性突触。靶向激活lh小胶质细胞逆转EA的抑制作用，从而增加LHGlu神经元活性，引发交感神经系统（SNS）过度激活，最终加重MIRI。结论EA-pre可抑制MIRI小鼠LHGlu神经元周围抑制性突触的小胶质吞噬，从而抑制LHGlu神经元活性，减少SNS输出，最终发挥心脏保护作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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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.