Key Laboratory of Acupuncture and Medicine Research of Ministry of Education Nanjing University of Chinese Medicine, Nanjing 210023, China.
The Second People's Hospital of Qidong, South Ring Road No. 229, Lvsigang Town, Qidong, Jiangsu Province 226200, China.
Mediators Inflamm. 2024 Jun 30;2024:8237681. doi: 10.1155/2024/8237681. eCollection 2024.
Electroacupuncture (EA) at the Neiguan acupoint (PC6) has shown significant cardioprotective effects. Sympathetic nerves play an important role in maintaining cardiac function after myocardial infarction (MI). Previous studies have found that EA treatment may improve cardiac function by modulating sympathetic remodeling after MI. However, the mechanism in how EA affects sympathetic remodeling and improves cardiac function remains unclear. The aim of this study is to investigate the cardioprotective mechanism of EA after myocardial ischemic injury by improving sympathetic remodeling and promoting macrophage M2 polarization. We established a mouse model of MI by occluding coronary arteries in male C57/BL6 mice. EA treatment was performed at the PC6 with current intensity (1 mA) and frequency (2/15 Hz). Cardiac function was evaluated using echocardiography. Heart rate variability in mice was assessed via standard electrocardiography. Myocardial fibrosis was evaluated by Sirius red staining. Levels of inflammatory factors were assessed using RT-qPCR. Sympathetic nerve remodeling was assessed through ELISA, western blotting, immunohistochemistry, and immunofluorescence staining. Macrophage polarization was evaluated using flow cytometry. Our results indicated that cardiac systolic function improved significantly after EA treatment, with an increase in fractional shortening and ejection fraction. Myocardial fibrosis was significantly mitigated in the EA group. The sympathetic nerve marker tyrosine hydroxylase and the nerve sprouting marker growth-associated Protein 43 were significantly reduced in the EA group, indicating that sympathetic remodeling was significantly reduced. EA treatment also promoted macrophage M2 polarization, reduced levels of inflammatory factors TNF-, IL-1, and IL-6, and decreased macrophage-associated nerve growth factor in myocardial tissue. To sum up, our results suggest that EA at PC6 attenuates sympathetic remodeling after MI to promote macrophage M2 polarization and improve cardiac function.
电针内关穴（PC6）具有显著的心脏保护作用。交感神经在心肌梗死后维持心脏功能中起着重要作用。先前的研究发现，电针治疗可能通过调节心肌梗死后的交感神经重塑来改善心脏功能。然而，电针对交感神经重塑和改善心脏功能的影响机制尚不清楚。本研究旨在通过改善交感神经重塑和促进巨噬细胞 M2 极化来探讨电针对心肌缺血损伤的心脏保护机制。我们通过结扎雄性 C57/BL6 小鼠冠状动脉建立心肌梗死模型。电针治疗在 PC6 穴位进行，电流强度为 1 mA，频率为 2/15 Hz。通过超声心动图评估心脏功能。通过标准心电图评估小鼠心率变异性。通过天狼猩红染色评估心肌纤维化。通过 RT-qPCR 评估炎症因子水平。通过 ELISA、western blot、免疫组化和免疫荧光染色评估交感神经重塑。通过流式细胞术评估巨噬细胞极化。我们的结果表明，电针治疗后心脏收缩功能显著改善，表现为缩短分数和射血分数增加。电针组心肌纤维化明显减轻。交感神经标志物酪氨酸羟化酶和神经发芽标志物生长相关蛋白 43 在电针组明显减少，表明交感神经重塑明显减少。电针治疗还促进了巨噬细胞 M2 极化，降低了心肌组织中 TNF-α、IL-1 和 IL-6 等炎症因子的水平，并减少了巨噬细胞相关的神经生长因子。综上所述，我们的结果表明，PC6 电针对 MI 后交感神经重塑具有抑制作用，可促进巨噬细胞 M2 极化，改善心脏功能。
