Electroacupuncture attenuates PVN-SCG sympathetic hyperactivation to improve cardiac function in myocardial...

Myocardial infarction (MI) triggers maladaptive sympathetic overactivation, which acts as a key driver of adverse cardiac remodeling and progression to heart failure. Electroacupuncture (EA) at the Neiguan (PC6) acupoint exhibits reliable cardioprotective effects, yet its central neural mechanisms remain incompletely clarified. This study investigated whether EA at PC6 improves post-MI outcomes by modulating the hypothalamic paraventricular nucleus-superior cervical ganglion (PVN-SCG) sympathetic axis. MI was surgically induced by permanent ligation of the left anterior descending coronary artery in mice, followed by consecutive EA treatment at PC6. Cardiac function was assessed by echocardiography, while sympathetic activity was evaluated via heart rate variability (HRV) analysis and norepinephrine levels of serum and heart. Myocardial fibrosis and key molecular markers within the PVN-SCG axis were systematically analyzed. In this mice MI model, EA at PC6 significantly improved cardiac function as indicated by ejection fraction and attenuated ventricular dilation. Mechanistically, EA suppressed systemic sympathetic activity, as evidenced by decreased serum and cardiac norepinephrine levels as well as normalized HRV parameters. Notably, EA markedly inhibited neuronal hyperactivity (c-fos expression) in both the PVN and SCG. Peripherally, EA mitigated cardiac sympathetic remodeling by downregulating tyrosine hydroxylase (TH) and synaptophysin (SYN) expression, accompanied by reduced myocardial fibrosis and collagen deposition. These findings demonstrate that EA at PC6 exerts s potent cardioprotection against post-MI injury by specifically inhibiting sympathetic hyperactivation at both central (PVN-SCG axis) and peripheral levels. This study identifies a novel neuromodulatory mechanism underlying EA therapy and supports PC6 EA as a promising non-pharmacological strategy for post-MI cardiac protection.