Electroacupuncture Pretreatment Alleviates Myocardial Ischemia-Reperfusion Injury by Inhibiting Engulfment

Xiang Zhou1,2, Peiyi Yang3, Chaonan Dong3

  • 1College of Traditional Chinese Medicine, Anhui University of Chinese Medicine, Hefei, China.

PubMed
Abstract

Insights

Electroacupuncture pretreatment (EA-pre) protects against myocardial ischemia-reperfusion injury (MIRI) by modulating microglia in the lateral hypothalamus. This treatment reduces neuroinflammation and sympathetic nervous system overactivation, offering a potential therapeutic strategy for MIRI.

Area of Science:

  • Neuroscience
  • Cardiology
  • Immunology

Background:

  • Myocardial ischemia-reperfusion injury (MIRI) involves neuroinflammation, particularly microglial activation.
  • Current clinical strategies for preventing MIRI remain unclear.
  • Microglia and glutamate (Glu) neurons in the lateral hypothalamus (LH) are implicated in MIRI pathogenesis.

Purpose of the Study:

  • To investigate electroacupuncture pretreatment (EA-pre) as a therapeutic strategy for MIRI.
  • To elucidate the underlying mechanisms of EA-pre in alleviating MIRI, focusing on LH microglia and Glu neurons.
  • To identify potential therapeutic targets for MIRI prevention.

Main Methods:

  • Establishment of a MIRI mouse model via coronary artery ligation and reperfusion.
  • Immunofluorescence staining to assess microglial activation in the LH.
  • Chemogenetics and fiber photometry recordings to investigate neuronal activity and microglial function.
  • Analysis of synaptic changes and sympathetic nervous system (SNS) output.

Main Results:

  • EA-pre significantly improved cardiac function in MIRI mice.
  • EA-pre suppressed microglial activation and reduced the engulfment of inhibitory synapses around LH Glu neurons.
  • Targeted activation of LH microglia reversed the protective effects of EA-pre, exacerbating MIRI via increased SNS activity.

Conclusions:

  • EA-pre exerts cardioprotective effects against MIRI by inhibiting microglial activity in the LH.
  • The mechanism involves preserving inhibitory synapses on LH Glu neurons, thereby reducing SNS overactivation.
  • Modulating LH microglia represents a promising therapeutic approach for MIRI.

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