Zhou Xiang, Yang Peiyi, Dong Chaonan, Chang Huimin, Zhang Fan, Shu Qi, Wei Naixuan, Zhang Bin, Wu Yan, Shao Wenjing, Cai Ronglin, Yu Qing
College of Traditional Chinese Medicine, Anhui University of Chinese Medicine, Hefei, China.
Anhui Wannan Rehabilitation Hospital (The Fifth People's Hospital of Wuhu), Chinese Medicine Rehabilitation Department, Wuhu, Anhui Province, China.
CNS Neurosci Ther. 2025 Sep;31(9):e70595. doi: 10.1111/cns.70595.
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.
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).
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 neurons. Targeted activation of LH reverses EA's inhibitory effect, thereby increasing LH neuronal activity and triggering overactivation of the sympathetic nervous system (SNS), which ultimately exacerbates MIRI.
EA-pre inhibits microglial engulfment of inhibitory synapses around LH neurons in MIRI mice, thereby suppressing LH neuronal activity, reducing SNS output, and ultimately exerting cardioprotective effects.
心肌缺血再灌注损伤（MIRI）的发生伴随着神经炎症反应，且与小胶质细胞过度激活密切相关。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）对MIRI的潜在治疗靶点及机制。
通过结扎心脏左前降支30分钟并再灌注2小时建立MIRI小鼠模型。通过免疫荧光染色、化学遗传学和纤维光度记录研究EA-pre减轻MIRI的机制，重点关注下丘脑外侧区（LH）中小胶质细胞和谷氨酸（Glu）能神经元的潜在作用。
EA-pre通过抑制LH区小胶质细胞激活改善MIRI小鼠的心功能。其潜在机制可能涉及EA-pre抑制小胶质细胞对LH神经元周围抑制性突触的吞噬。靶向激活LH可逆转EA的抑制作用，从而增加LH神经元活动并触发交感神经系统（SNS）过度激活，最终加重MIRI。
EA-pre抑制MIRI小鼠LH神经元周围抑制性突触的小胶质细胞吞噬，从而抑制LH神经元活动，减少SNS输出，最终发挥心脏保护作用。
