Iranian Journal of Basic Medical Sciences

Iranian Journal of Basic Medical Sciences

Electroacupuncture preconditioning alleviates myocardial ischemia-reperfusion injury through reducing the inflammatory response mediated by the miR-146a/TRAF6/IRAK4 pathway

Document Type : Original Article

Authors
1 Academy of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
2 Department of Anatomy, School of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
3 Department of General Practice, Yuepu Town Community Health Service Center, Shanghai 200941, China
4 School of Nursing, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
5 Department of Histoembryology, School of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
10.22038/ijbms.2026.94614.20408
Abstract
Objective(s): Myocardial ischemia-reperfusion injury (MIRI) lacks effective multi-target interventions. Electroacupuncture (EA) shows cardioprotective potential, but its molecular mechanisms remain incompletely understood. This study aimed to investigate whether EA exerts cardioprotective effects by modulating myocardial miR-146a, a microRNA closely associated with inflammation and cardiovascular diseases.
Materials and Methods: A rat model of MIRI was established, and Sprague-Dawley rats were divided into four groups: sham, MIRI, EA treatment, and miR-146a inhibition+EA. Cardiac function, infarct size, myocardial injury, apoptosis, and inflammatory cytokine levels were assessed using echocardiography, TTC staining, CK and LDH assays, TUNEL staining, and ELISA, respectively. The expression and cellular origin of miR-146a were assessed via qRT-PCR, in situ hybridization, and immunofluorescence.
Results: EA treatment significantly improved cardiac function, reduced infarct size, attenuated myocardial injury and apoptosis, and upregulated miR-146a expression in cardiomyocytes. In contrast, inhibition of miR-146a markedly attenuated the protective effects of EA and down-regulated the expression of angiogenic factors bFGF and VEGF, while compromising its anti-inflammatory actions. Furthermore, EA-mediated down-regulation of the inflammatory response was mediated through the miR-146a/TRAF6/IRAK4 pathway.
Conclusion: These findings suggest that EA may alleviate MIRI by upregulating myocardial miR-146a expression, providing novel molecular insights into the cardioprotective mechanisms of EA.
Keywords
Subjects

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Articles in Press, Accepted Manuscript
Available Online from 31 August 2026