ArticleExperimental and therapeutic medicine2016
Vagus nerve stimulation attenuates myocardial ischemia/reperfusion injury by inhibiting the expression of interleukin-17A.
Article in Experimental and therapeutic medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- The mechanism and clinical research of vagus nerve electrical stimulation in the treatment of myocardial ischemia-reperfusion injury.iScience · 2026Review
- Electrical Vagus Nerve Stimulation Ameliorates Cardiac Ischemia and Reperfusion Injury by Improving Mitochondrial Biogenesis Through the SIRT1/PGC-1α Pathway.Applied biochemistry and biotechnology · 2025Article
- Preoperative transcutaneous vagus nerve stimulation as a novel strategy to prevent postoperative atrial fibrillation in calcific aortic valve disease: mechanistic insights and translational perspectives.Frontiers in cardiovascular medicine · 2025Review
- Neuromodulatory co-expression in cardiac vagal motor neurons of the dorsal motor nucleus of the vagus.iScience · 2024Article
- Vagus Nerve Stimulation and Inflammation in Cardiovascular Disease: A State-of-the-Art Review.Journal of the American Heart Association · 2023Review
- Vagus Nerve Stimulation and Its Cardioprotective Abilities: A Systematic Review.Journal of clinical medicine · 2023Review
- The protective effect of vagus nerve stimulation against myocardial ischemia/reperfusion injury: pooled review from preclinical studies.Frontiers in pharmacology · 2023Article
- Transcutaneous auricular vagus nerve stimulation in poststroke cognitive impairment: protocol for a randomised controlled trial.BMJ open · 2022Article
- Stress and the "extended" autonomic system.Autonomic neuroscience : basic & clinical · 2021Review
- The extended autonomic system, dyshomeostasis, and COVID-19.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2020Review
- Auricular Vagus Nerve Stimulation Exerts Antiinflammatory Effects and Immune Regulatory Function in a 6-OHDA Model of Parkinson's Disease.Neurochemical research · 2018Article
- Vagus Nerve Stimulation for Treatment of Inflammation: Systematic Review of Animal Models and Clinical Studies.Bioelectronic medicine · 2016Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-17A has an important role in myocardial ischemia/reperfusion (I/R) injury, and vagal stimulation (VS) has been demonstrated to exert cardioprotective effects. The present study aimed to investigate the effects of VS on a rat model of myocardial I/R injury, and detected an association between VS and IL-17A. Anesthetized rats underwent VS (2 msec; 10 Hz) or were treated with anti-IL-17A neutralized monoclonal antibodies (mAbs) (200 µg; iv), and subjected to ischemia for 30 min prior to 4 h reperfusion. The following parameters were measured: Infarct size; lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) and caspase-3 activity levels; tumor necrosis factor (TNF)-α and IL-6 expression levels; and the percentage of terminal deoxynucleotidyl-transferase mediated dUTP nick-end labeling (TUNEL) positive cells. High mobility group box 1 protein (HMGB1) and IL-17A expression levels were assessed by immunoblotting. Following 4 h reperfusion, VS was able to significantly decrease the infarct size and the activity levels of LDH and CK (P<0.05). Furthermore, VS administration significantly suppressed the increased MDA and decreased SOD activity levels, and significantly reduced caspase-3 activity and the percentage of TUNEL-positive cells (P<0.05). Treatment with anti-IL-17A mAbs demonstrated the same effects as VS. Furthermore, VS was able to significantly inhibit the increased expression levels of TNF-α, IL-6, HMGB1 and IL-17A induced by I/R (P<0.05). The results of the present study suggested that VS may attenuate myocardial I/R injury by reducing the expression of inflammatory cytokines, oxidative stress and the apoptosis of cardiomyocytes. Furthermore, VS may induce cardioprotective effects, which may be associated with the inhibition of IL-17A expression.
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