ArticleExperimental and therapeutic medicine2015
Preconditioning with PEP-1-SOD1 fusion protein attenuates ischemia/reperfusion-induced ventricular arrhythmia in isolated rat hearts.
Article in Experimental and therapeutic medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- Arrhythmogenic Mechanisms of Novel Biomarkers in Cardiac Electrophysiology.Cardiology research and practice · 2026Review
- Transduction of jellyfish superoxide dismutase mediated by TAT peptide ameliorates HScientific reports · 2024Article
- Protective effects of gallic acid on cardiac electrophysiology and arrhythmias during reperfusion in diabetes.Iranian journal of basic medical sciences · 2019Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PEP 1-Cu/Zn superoxide dismutase (PEP-1-SOD1) fusion protein preconditioning has been reported to protect the myocardium from ischemia/reperfusion (I/R)-induced injury by decreasing the infarct size, reducing levels of cardiomyocyte apoptosis and reducing the release of myocardial-specific biomarkers. The aim of the present study was to examine the effects of PEP-1-SOD1 pretreatment on I/R-induced ventricular arrhythmias in Langendorff-perfused rat hearts. The isolated rat hearts were pretreated with PEP-1-SOD1 prior to I/R, and the I/R-induced hemodynamic parameters, infarct size and ventricular arrhythmias were then assessed. Compared with the unprotected hearts, PEP-1-SOD1 preconditioning significantly improved the hemodynamic parameters, decreased the cardiac lactate dehydrogenase and creatine kinase-MB (CK-MB) levels, reduced the infarct size and attenuated the ventricular arrhythmia. Further investigation showed that PEP-1-SOD1 preconditioning reduced both the incidence and duration of ventricular tachycardia/ventricular fibrillation. In addition, the intracellular reactive oxygen species (ROS) levels were decreased. The results of the present study suggest that PEP-1-SOD1 preconditioning can protect the heart against I/R injury and attenuate I/R-induced arrhythmia by downregulating the generation of ROS.
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