Bai Hua, Xu Sen-Lei, Shi Jun-Jing, Ding Ya-Ping, Liu Qiong-Qiong, Jiang Chun-Hong, He Li-Li, Zhang Hong-Ru, Lu Sheng-Feng, Gu Yi-Huang
Key Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Acupuncture and Tuina College, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Heliyon. 2023 Aug 29;9(9):e19396. doi: 10.1016/j.heliyon.2023.e19396. eCollection 2023 Sep.
The protective effects of electroacupuncture (EA) preconditioning against myocardial ischemia-reperfusion injury (MIRI) have been reported. However, the underlying mechanism remains unclear. Recent research has indicated that the dynamic inflammatory response following MIRI plays an essential role in the progression of myocardial injury. This study aimed to investigate the myocardial protective effects of EA preconditioning on MIRI in rats and to explore the relevant mechanism from the perspective of dynamic inflammatory response.
A MIRI model was employed, and the rats were subjected to EA on Neiguan for four days prior to modeling. The myocardial protective effect of EA preconditioning was evaluated by echocardiography, Evans blue and triphenyltetrazolium chloride staining. Real-time polymerase chain reaction, Western blot, hematoxylin & eosin staining, and immunohistochemistry were utilized to detect the content of mitochondrial DNA, NOD receptor family protein 3 (NLRP3) inflammasome activation, neutrophil recruitment and macrophage infiltration in blood samples and myocardium below the ligation.
We found that EA preconditioning could accelerate the recovery of left ventricle function after MIRI and reduce the myocardial infarction area, thereby protecting the myocardium against MIRI. Furthermore, EA preconditioning was observed to ameliorate mitochondrial impairment, reduce the level of plasma mitochondrial DNA, modulate NLRP3 inflammasome activation, attenuate neutrophil infiltration, and promote the polarization of M1 macrophages towards M2 macrophages in the myocardium after MIRI.
EA preconditioning could reduce plasma mtDNA, suppress overactivation of the NLRP3 inflammasome, facilitate the transition from the acute pro-inflammatory phase to the anti-inflammatory reparative phase after MIRI, and ultimately confer cardioprotective benefits.
电针（EA）预处理对心肌缺血再灌注损伤（MIRI）具有保护作用，这一点已有报道。然而，其潜在机制仍不清楚。最近的研究表明，MIRI后的动态炎症反应在心肌损伤进展中起着至关重要的作用。本研究旨在探讨EA预处理对大鼠MIRI的心肌保护作用，并从动态炎症反应的角度探索相关机制。
采用MIRI模型，在建模前4天对大鼠内关穴进行电针治疗。通过超声心动图、伊文思蓝和氯化三苯基四氮唑染色评估EA预处理的心肌保护作用。利用实时聚合酶链反应、蛋白质免疫印迹法、苏木精-伊红染色和免疫组织化学检测血液样本和结扎部位以下心肌中线粒体DNA含量、NOD样受体家族蛋白3（NLRP3）炎性小体激活、中性粒细胞募集和巨噬细胞浸润情况。
我们发现EA预处理可加速MIRI后左心室功能的恢复，减小心肌梗死面积，从而保护心肌免受MIRI损伤。此外，观察到EA预处理可改善线粒体损伤，降低血浆线粒体DNA水平，调节NLRP3炎性小体激活，减轻中性粒细胞浸润，并促进MIRI后心肌中M1巨噬细胞向M2巨噬细胞极化。
EA预处理可降低血浆线粒体DNA水平，抑制NLRP3炎性小体过度激活，促进MIRI后从急性促炎阶段向抗炎修复阶段的转变，并最终带来心脏保护益处。
