ORIGINAL RESEARCH article
Front. Cardiovasc. Med.
Sec. Cardiovascular Pharmacology and Drug Discovery
Volume 12 - 2025 | doi: 10.3389/fcvm.2025.1628940
Salidroside ameliorates abnormalities in electrophysiological indices induced by perfusion of the heart with low-potassium solutions
Provisionally accepted
- 1The First Affiliated Hospital of Xinxiang Medical University, xinxaing, China
- 2Department of Research, Scope Research Institute of Electrophysiology, Kaifeng, China
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Malignant arrhythmias related to hypokalemia are a key risk factor for cardiac arrest, but the specific mechanism remains unclear. In this study, using electrophysiological mapping and transcriptomics techniques, the effects of hypokalemia and paclitaxel (SAL) on isolated rat hearts were investigated. Hypokalemia (3.5-2.0 mmol/L) dose-dependently triggered abnormal arrhythmias and increased the incidence of arrhythmias, while SAL (5ug/ml) improved this situation. Transcriptomics revealed that hypokalemia upregulated Mt-nd6 and disrupted the inflammatory/immune pathways, while SAL reversed these changes and activated PPAR-related genes. SAL improves the electrophysiological abnormalities caused by hypokalemia by regulating inflammation, immunity and energy metabolism, and has the potential to treat related arrhythmias.
Keywords: Hypokalaemia, Salidroside, Transcriptomic Analysis, Cardiac Electrophysiology, arrhythmia
Received: 15 May 2025; Accepted: 29 Jul 2025.
Copyright: © 2025 Yang, Zhou, Yan, Li, Wang, Li, Lin and Hao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Fei Lin, The First Affiliated Hospital of Xinxiang Medical University, xinxaing, China
Guoliang Hao, Department of Research, Scope Research Institute of Electrophysiology, Kaifeng, China
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