Electroacupuncture Protects Against Post-MI Heart Failure Through Autonomic Regulation and α7nAChR Activation.

OBJECTIVE

This study investigated whether electroacupuncture (EA) at Neiguan (PC6) acupoint alleviates adverse myocardial remodeling in post-myocardial infarction (MI) heart failure (HF) by activating the vagus nerve-mediated cholinergic pathway and its downstream α7nAChR-Akt-HIF-1α-VEGF signaling cascade.

METHODS

Male Sprague Dawley (SD) rats were randomized into sham, MI model, and EA groups (n = 6 per group). MI was induced by ligation of the left anterior descending coronary artery. EA was applied at PC6 for 14 days starting 1 week after MI induction. Cardiac function and structure were evaluated using echocardiography and histological examination. The expression levels of choline acetyltransferase (ChAT), α7-nicotinic acetylcholine receptor (α7nAChR), phosphorylated Akt (p-Akt), hypoxia-inducible factor-1α (HIF-1α), and vascular endothelial growth factor (VEGF) were analyzed by real-time quantitative PCR, Western blotting, and immunohistochemistry.

RESULTS

EA intervention significantly attenuated pathological myocardial remodeling and improved cardiac function. Compared with the model group, EA treatment markedly enhanced cardiac function, increased contractility, reduced ventricular dilation, restored autonomic balance, and alleviated myocardial necrosis and fibrosis. Molecular studies revealed that EA treatment increased the expression of ChAT and α7nAChR, elevated p-Akt levels, and upregulated the expression of HIF-1α and VEGF. These findings suggest the activation of the vagus nerve-cholinergic signaling pathway and its downstream prosurvival and pro-angiogenic pathways.

CONCLUSIONS

EA attenuated maladaptive ventricular remodeling and improved cardiac performance. These effects were associated with modulation of autonomic function and engagement of the α7nAChR/Akt/HIF-1α/VEGF signaling axis, supporting a potential neuro-immune-angiogenic mechanism underlying EA-mediated myocardial repair during the subacute post-MI phase.