Volume 39 Issue 4
Apr.  2023
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Article Navigation >  Journal of Nanjing University of traditional Chinese Medicine  > 2023  >  39(4): 319-327
SHI Jun-jing, YANG Jia-li, MA Nai-qi, JIANG Min-Jiao, PENG Rou, FU Shu-ping, BAI Hua, YU Mei-ling, LU Sheng-feng. Electroacupuncture Influences Macrophage M2 Polarization and TLR4 and MyD88 Expression in Myocardial Tissue of Myocardial Ischemia Injury Mice[J]. Journal of Nanjing University of traditional Chinese Medicine, 2023, 39(4): 319-327. doi: 10.14148/j.issn.1672-0482.2023.0319
Citation: SHI Jun-jing, YANG Jia-li, MA Nai-qi, JIANG Min-Jiao, PENG Rou, FU Shu-ping, BAI Hua, YU Mei-ling, LU Sheng-feng. Electroacupuncture Influences Macrophage M2 Polarization and TLR4 and MyD88 Expression in Myocardial Tissue of Myocardial Ischemia Injury Mice[J]. Journal of Nanjing University of traditional Chinese Medicine, 2023, 39(4): 319-327. doi: 10.14148/j.issn.1672-0482.2023.0319
shu

Electroacupuncture Influences Macrophage M2 Polarization and TLR4 and MyD88 Expression in Myocardial Tissue of Myocardial Ischemia Injury Mice

doi: 10.14148/j.issn.1672-0482.2023.0319
  • 1.

    Key Laboratory of Acupuncture and Medicine Research of Ministry of Education, Nanjing University of Chinese Medicine, Nanjing 210023, China

  • 2.

    School of Elderly Care Services and Management, Nanjing University of Chinese Medicine, Nanjing 210023, China

  • Received Date: 2022-11-01
    Available Online: 2023-04-17
    Abstract
  •   OBJECTIVE  To observe the effect of electroacupuncture on cardiac function and its effect on macrophage polarization, TLR4 and MyD88 expression in the heart of mice with myocardial infarction, and to explore the possible mechanism of electroacupuncture against cardioprotection.  METHODS  27 male C57BL/6J mice were randomly divided into the sham-operated group, model group, and electroacupuncture group, with 9 mice in each group. The myocardial ischemia model was established by ligating the left anterior descending branch of the coronary artery in the model group and electroacupuncture group. In the electroacupuncture group, after successful modeling, the mice were treated with electroacupuncture at the bilateral Neiguan points: 2/15 Hz, dense and sparse waves, 1 mA, 20 min/time, once a day for 7 days. The ejection fraction (EF) and short-axis systolic rate (FS) were calculated by echocardiography; the fibrosis of mice heart was observed by Sirius red staining; the number of neutrophils and macrophages in myocardial tissue and the percentage of macrophages in each phenotype was detected by flow cytometry; the mRNA expression of TNF-α and IL-1β in myocardial tissue were detected by real-time quantitative fluorescence PCR; the protein expression levels of TLR4, MyD88, IL-1β, and IL-17A in myocardial tissues were detected by Western blot.  RESULTS  Compared with the sham-operated group, mice in the model group showed decreased EF and FS values (P < 0.0001), increased collagen volume fraction (P < 0.001), increased numbers of neutrophils and macrophages in cardiac tissues (P < 0.0001, P < 0.001), as well as increased percentage of M1-type macrophages (P < 0.05). The mRNA expression of TNF-α, IL-1β in myocardial tissues expression increased (P < 0.01, P < 0.001); TLR4, MyD88, IL-1β, IL-17A protein expression levels increased (P < 0.05, P < 0.01); compared with the model group, mice in the electroacupuncture group had higher EF and FS values (P < 0.01, P < 0.001), lower collagen volume fraction (P < 0.001), the numbers of neutrophils and macrophages in cardiac tissues decreased (P < 0.0001, P < 0.01), while the percentage of M2-type macrophages increased (P < 0.05), the mRNA expression of TNF-α and IL-1β in myocardial tissues decreased (P < 0.001), and the TLR4, MyD88, IL-1β, IL-17A protein expression levels were decreased (P < 0.05, P < 0.001).  CONCLUSION  Electroacupuncture may achieve myocardial protective effects by reducing the expression of TLR4 and MyD88 in myocardial tissue, promoting the polarization of cardiac macrophages to M2 type after MI, reducing local inflammation, and inhibiting myocardial fibrosis.

     

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