3.8 Article

Mechanisms of Electroacupuncture Pretreatment in Alleviating Myocardial Ischemia Reperfusion Injury: Interactions between the Cerebellar Fastigial Nucleus and Lateral Hypothalamic Area

Journal

JOURNAL OF ACUPUNCTURE AND MERIDIAN STUDIES
Volume 14, Issue 6, Pages 207-218

Publisher

MEDICAL ASSOC PHARMACOPUNCTURE INST-MAPI
DOI: 10.51507/j.jams.2021.14.6.207

Keywords

Electroacupuncture; Lateral hypothalamic area; Cerebellar fastigial nucleus; Myocardial ischemia reperfusion injury; Heart meridian

Funding

  1. National Natural Science Foundation of China [81774414, 8197375, 82074536, 82104999]
  2. Project for the Cultivation of Outstanding and Top Talents in Universities of Anhui Province [gxgwfx2019025]
  3. Nature Science Research Project of Anhui Province [2108085Y30, 2108085QH364]

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This study found that electroacupuncture (EA) pretreatment can reduce ST-segment elevation, arrhythmia scores, and morphological changes in MIRI myocardial cells in rats, and decrease c-fos protein expression in LHA/FN nuclei. MIRI is associated with an imbalance between GABA and Glu levels, while EA pretreatment increases GABA levels and decreases Glu levels in the LHA/FN, suggesting that FN and LHA are involved in the EA-mediated attenuation of MIRI.
Background: Myocardial ischemia reperfusion injury (MIRI) is an important mechanism of post-myocardial infarction injury and a main cause of death in patients with ischemic heart disease. Electroacupuncture (EA) pretreatment is effective for the prevention and treatment of MIRI, but mechanisms mediating the effects of cardiovascular disease EA treatments remain unclear. Objectives: To determine whether the lateral hypothalamus (LHA) and the cerebellar fastigial nucleus (FN) are involved in the protective effects of EA stimulation on MIRI. Methods: EA pretreatment was performed for 7 days before the establishment of the MIRI model. ST-segment changes on electrocardiograms were recorded and the Curtis-Walker arrhythmia score was used to evaluate changes in reperfusion injury. Hematoxylin-eosin staining was applied to evaluate the pathological and morphological changes in myocardial tissue. c-fos expression in the LHA and FN was determined by immunofluorescence staining. Glutamic (Glu) and y-Aminobutyric acid (GABA) levels were measured using a high-performance liquid chromatography-electrochemical method. Results: EA pretreatment reduced ST-segment elevation, arrhythmia scores, and morphological changes in MIRI myocardial cells in rats, and decreased the c-fos protein expression in LHA/FN nuclei. MIRI was associated with an imbalance between GABA and Glu levels, whereas EA pretreatment increased GABA levels and decreased Glu levels in the LHA/FN. Conclusion: FN and LHA are involved in the EA-mediated attenuation of MIRI. Pretreatment with EA plays a protective role in the myocardium by regulating Glu and GABA release in the LHA and FN.

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