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Electroacupuncture preconditioning at PC6 or ST36 alleviates myocardial inflammation and promotes M2 macrophage
Liyao Chen1,2, Wenxiu Yang3, Junjing Shi4
1Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, China.
Background:
Acupuncture at different traditional acupuncture point locations activates different autonomic pathways and modulates systemic inflammation. Electroacupuncture preconditioning (EAP) at PC6 or ST36 has been demonstrated to be cardioprotective during acute myocardial ischemia (MI) injury, but the mechanism remains unclear. As inflammation is crucial for repair post-MI, we aimed to investigate whether the protective effect of EAP at PC6 or ST36 is related to the suppression of inflammation and whether autonomic pathways are involved.
Methods:
Mice underwent ligation of the left anterior descending (LAD) coronary artery to generate model MI after 3 days of EAP at PC6 or ST36. Echocardiography and triphenyltetrazolium chloride (TTC) staining were used to evaluate cardiac function and myocardial infarction area. Cardiac troponin (cTn)I and norepinephrine (NE) were measured by enzyme-linked immunosorbent assay (ELISA). Flow cytometry was employed to determine macrophage M1/M2 phenotypic polarization, and the levels of pro- and anti-inflammatory cytokines in cardiac tissue were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). In addition, unilateral cervical vagotomy and chemical sympathetic blockade were employed to clarify specific autonomic pathways.
Results:
EAP at PC6 or ST36 preserved cardiac function, reduced myocardial infarct size, decreased serum cTnI levels, promoted M2 macrophage polarization and decreased the cardiac pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-18 and nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3). Compared to EAP at ST36, EAP at PC6 yielded a better cardioprotective effect and regulated the anti-inflammatory cytokine transforming growth factor (TGF)-β. Moreover, sympathetic nerves were involved in the protective effect of EAP at PC6, while the vagus nerve was necessary for EAP at ST36.
Conclusion:
Our findings suggest that EAP at PC6 or ST36 activates different autonomic pathways and modulates M2 macrophage polarization, resulting in the suppression of myocardial inflammation.
