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Peer-reviewedCC BY 4.0Frontiers in Physiology

Electroacupuncture pretreatment attenuates myocardial ischemia/reperfusion injury-induced ferroptosis via the p53/SLC7A11/GPX4 pathway

  • Jing Mao1
  • Qian-Ru Guo2
  • Yi-Pu Luo1
  • Cong-Fei Liu1
  • Zhen-Yang Cao1
  • Yun-Tao Yu1
  • Wen-Wei Wu1
  • Xin-Yu Luan1
  • Dan-Ning Xu1
  • Hua Wang1
  • Pu Chen3
  • Song Wu1
  1. 1Department of Acupuncture-Moxibustion and Orthopedics, Hubei University of Chinese Medicine, Wuhan, China
  2. 2The First Clinical College of Hubei University of Chinese Medicine, Wuhan, China
  3. 3Hubei Shizhen Laboratory, Wuhan, China
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Abstract

Introduction: A major side effect of reperfusion therapy after myocardial infarction is myocardial ischemia-reperfusion injury (MIRI). Electroacupuncture (EA) preconditioning has a long history of application in the treatment of cardiovascular diseases. This study aims to investigate whether EA preconditioning alleviates MIRI by regulating the p53/SLC7A11/GPX4 pathway to suppress the ferroptotic biochemical phenotype characterized by iron accumulation and lipid peroxidation.

Methods: Healthy male SPF rats were randomly divided into nine groups: Ctrl, Sham, MIRI, EA, RSL-3+EA, COTI-2+EA, Erastin+EA, COTI-2+Erastin+EA, and COTI-2+Pantethine+EA. Before MIRI induction, EA pretreatment was applied daily at CV4, bilateral ST36, and bilateral PC6 for 20 min (2 Hz, 1 mA) for 7 consecutive days. Pharmacological interventions were administered intraperitoneally once daily for 7 consecutive days before EA stimulation. The MIRI model was established by ligating the left anterior descending coronary artery for 30 min followed by 2 h of reperfusion. Myocardial oxidative stress, ferroptosis-related markers, myocardial injury markers, and cardiomyocyte apoptosis were assessed using corresponding commercial kits, DCFH-DA probe combined with flow cytometry, RhoNox-6 fluorescent probe, Western blot, RT-PCR, ELISA, and TUNEL staining combined with flow cytometry.

Results: EA preconditioning inhibited p53 expression, promoted the activation of the SLC7A11/GPX4 pathway, and thereby alleviated myocardial injury. The morphology of cardiomyocytes in EA-pretreated rats was altered, and the apoptosis rate of cardiomyocytes in these rats was also reduced. In addition, administration of Erastin (SLC7A11 inhibitor) showed effects similar to those of COTI-2 (p53 agonist) intervention, whereas pantethine (SLC7A11 agonist) reversed the effects of COTI-2, exerting anti-ferroptotic and cardioprotective effects.

Discussion: As a proof‑of‑concept study with limited sample size per experimental group, our findings preliminarily suggest that EA preconditioning ameliorates MIRI by suppressing the ferroptotic biochemical signature characterized by myocardial iron overload and lipid peroxidation through the p53/SLC7A11/GPX4 pathway. Further studies with larger sample sizes are still needed for validation.

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Cite

BibTeXRIS
BibTeX
@article{mao2026electroacupuncture,
  title = {{Electroacupuncture pretreatment attenuates myocardial ischemia/reperfusion injury-induced ferroptosis via the p53/SLC7A11/GPX4 pathway}},
  author = {Jing Mao and Qian-Ru Guo and Yi-Pu Luo and Cong-Fei Liu and Zhen-Yang Cao and Yun-Tao Yu and Wen-Wei Wu and Xin-Yu Luan and Dan-Ning Xu and Hua Wang and Pu Chen and Song Wu},
  journal = {Frontiers in Physiology},
  year = {2026},
  month = oct,
  doi = {10.3389/fphys.2026.1928208},
  url = {https://doi.org/10.3389/fphys.2026.1928208},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Electroacupuncture pretreatment attenuates myocardial ischemia/reperfusion injury-induced ferroptosis via the p53/SLC7A11/GPX4 pathway
AU  - Jing Mao
AU  - Qian-Ru Guo
AU  - Yi-Pu Luo
AU  - Cong-Fei Liu
AU  - Zhen-Yang Cao
AU  - Yun-Tao Yu
AU  - Wen-Wei Wu
AU  - Xin-Yu Luan
AU  - Dan-Ning Xu
AU  - Hua Wang
AU  - Pu Chen
AU  - Song Wu
PY  - 2026
DA  - 2026/10/12
JO  - Frontiers in Physiology
DO  - 10.3389/fphys.2026.1928208
UR  - https://doi.org/10.3389/fphys.2026.1928208
AB  - Introduction: A major side effect of reperfusion therapy after myocardial infarction is myocardial ischemia-reperfusion injury (MIRI). Electroacupuncture (EA) preconditioning has a long history of application in the treatment of cardiovascular diseases. This study aims to investigate whether EA preconditioning alleviates MIRI by regulating the p53/SLC7A11/GPX4 pathway to suppress the ferroptotic biochemical phenotype characterized by iron accumulation and lipid peroxidation.  Methods: Healthy male SPF rats were randomly divided into nine groups: Ctrl, Sham, MIRI, EA, RSL-3+EA, COTI-2+EA, Erastin+EA, COTI-2+Erastin+EA, and COTI-2+Pantethine+EA. Before MIRI induction, EA pretreatment was applied daily at CV4, bilateral ST36, and bilateral PC6 for 20 min (2 Hz, 1 mA) for 7 consecutive days. Pharmacological interventions were administered intraperitoneally once daily for 7 consecutive days before EA stimulation. The MIRI model was established by ligating the left anterior descending coronary artery for 30 min followed by 2 h of reperfusion. Myocardial oxidative stress, ferroptosis-related markers, myocardial injury markers, and cardiomyocyte apoptosis were assessed using corresponding commercial kits, DCFH-DA probe combined with flow cytometry, RhoNox-6 fluorescent probe, Western blot, RT-PCR, ELISA, and TUNEL staining combined with flow cytometry.  Results: EA preconditioning inhibited p53 expression, promoted the activation of the SLC7A11/GPX4 pathway, and thereby alleviated myocardial injury. The morphology of cardiomyocytes in EA-pretreated rats was altered, and the apoptosis rate of cardiomyocytes in these rats was also reduced. In addition, administration of Erastin (SLC7A11 inhibitor) showed effects similar to those of COTI-2 (p53 agonist) intervention, whereas pantethine (SLC7A11 agonist) reversed the effects of COTI-2, exerting anti-ferroptotic and cardioprotective effects.  Discussion: As a proof‑of‑concept study with limited sample size per experimental group, our findings preliminarily suggest that EA preconditioning ameliorates MIRI by suppressing the ferroptotic biochemical signature characterized by myocardial iron overload and lipid peroxidation through the p53/SLC7A11/GPX4 pathway. Further studies with larger sample sizes are still needed for validation.
SN  - 1664-042X
ER  -