文章摘要
不同频率电针调控AMPK/PGC-1α通路改善慢性心肌缺血大鼠心肌损伤的机制研究
Mechanism Study of Electroacupuncture Preconditioning at Different Frequencies Regulating the AMPK/PGC-1α Pathway to Improve Myocardial Injury in Rats with Chronic Myocardial Ischemia
投稿时间:2026-07-23  修订日期:2026-07-27
DOI:
中文关键词: 电针  慢性心肌缺血  AMPK/PGC-1α通路  心肌损伤  频率依赖性
英文关键词: Electroacupuncture  Chronic myocardial ischemia  AMPK/PGC-1α signaling  Myocardial injury  Frequency-dependent
基金项目:
作者单位邮编
罗蒙 武汉市第三医院 湖北 武汉 430065
鲁晓玲 武汉市第三医院 湖北 武汉 
江波 武汉市第三医院 湖北 武汉 
孙勤国 武汉市第三医院 湖北 武汉 
蔡旭 武汉大学人民医院 湖北 武汉 湖北省妇幼保健院湖北省妇女儿童医院湖北 武汉 课题编号:武汉市卫生健康委科研项目WZZ 
周本宏 武汉大学人民医院 湖北 武汉 湖北省妇幼保健院湖北省妇女儿童医院湖北 武汉 课题编号:武汉市卫生健康委科研项目WZZ 
张林* 湖北省妇幼保健院(湖北省妇女儿童医院) 
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中文摘要:
  目的:探究不同频率电针通过调控AMPK/PGC-1α通路改善慢性心肌缺血大鼠心肌损伤的频率依赖性机制。方法:将75只SD大鼠随机分为空白对照、模型、低频(2Hz)、高频(100Hz)及假电针组;采用异丙肾上腺素连续注射构建慢性心肌缺血模型,进行10天电针处理。结果:与模型组比,低频和高频电针均改善大鼠状态,降低血清糖脂、心肌损伤标志物(LDH、CK-MB)及炎性因子(IL-6、IL-1β、TNF-α),提升心肌ATP含量并上调AMPK与PGC-1α表达(P<0.05)。低频电针保护作用及通路激活均优于高频(P<0.05),假电针组无改善。结论:电针可缓解心肌损伤,机制可能与激活AMPK/PGC-1α信号、优化能量代谢及抑制炎症有关,低频优势显著,为优化电针参数提供实验依据,提示低频电针可能为保护心肌线粒体功能的治疗策略。
英文摘要:
    Objective: To investigate the frequency-dependent mechanism by which electroacupuncture preconditioning at different frequencies improves myocardial injury in rats with chronic myocardial ischemia through regulating the AMPK/PGC-1α pathway. Methods: Seventy-five SD rats were randomly divided into blank control, model, low-frequency (2 Hz), high-frequency (100 Hz), and sham electroacupuncture groups. A chronic myocardial ischemia model was established by continuous injection of isoproterenol, followed by 10 days of electroacupuncture treatment. Results: Compared with the model group, both low-frequency and high-frequency electroacupuncture improved the general condition of rats, reduced serum glucose and lipid levels, myocardial injury markers (LDH, CK-MB), and inflammatory factors (IL-6, IL-1β, TNF-α), increased myocardial ATP content, and upregulated the expression of AMPK and PGC-1α (P<0.05). The protective effect and pathway activation of low-frequency electroacupuncture were superior to those of high-frequency electroacupuncture (P<0.05), while the sham electroacupuncture group showed no improvement. Conclusion: Electroacupuncture can alleviate myocardial injury, and the mechanism may be related to activating the AMPK/PGC-1α signaling, optimizing energy metabolism, and inhibiting inflammation. Low-frequency electroacupuncture shows significant advantages, providing experimental evidence for optimizing electroacupuncture parameters and suggesting that low-frequency electroacupuncture may be a therapeutic strategy for protecting myocardial mitochondrial function.
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