Literature DB >> 33390936

Pinocembrin Decreases Ventricular Fibrillation Susceptibility in a Rat Model of Depression.

Tianxin Ye1,2,3, Cui Zhang1,2,3, Gang Wu1,2,3, Weiguo Wan1,2,3, Yan Guo1,2,3, Yuhong Fo1,2,3, Xiuhuan Chen1,2,3, Xin Liu1,2,3, Qian Ran1,2,3, Jinjun Liang1,2,3, Shaobo Shi1,2,3, Bo Yang1,2,3.   

Abstract

Background: Depression is associated with the increased risk of mortality and morbidity and is an independent risk factor for many cardiovascular diseases. Depression may promote cardiac arrhythmias, but little is known about the mechanisms. Pinocembrin mitigated depressive-like behaviors and exhibited cardioprotective effects in several models; however, whether pinocembrin benefits ventricular arrhythmias in depression models has not been elucidated. Thus, this study was to evaluate the effects of pinocembrin on ventricular fibrillation susceptibility in rat models of depression.
Methods: Male Sprague-Dawley rats were randomly assigned into control, control + pinocembrin, MDD (major depressive disorder), and MDP (MDD + pinocembrin) groups, respectively. Depressive-like behaviors, ventricular electrophysiological parameters, electrocardiogram parameters, heart rate variability, ventricular histology, serum norepinephrine, tumor necrosis factor-α, and interleukin-1β were detected. Protein levels in left ventricle were measured by Western blot assays.
Results: Compared with the MDD group, pinocembrin significantly mitigated depressive-like behaviors, prolonged ventricular effective refractory period, action potential duration, QT, and corrected QT (QTc) interval, improved heart rate variability, decreased Tpeak-Tend interval, ventricular fibrillation inducibility rate, ventricular fibrosis, ventricular positive nerve densities, and protein expression of tyrosine hydroxylase and growth associated protein-43, reduced serum norepinephrine, tumor necrosis factor-α, interleukin-1β concentrations, and the expression levels of p-IκBα and p-p65, and increased the protein expression of Cx43, Cav1.2, and Kv.4.2 in the MDP group.
Conclusion: Pinocembrin attenuates ventricular electrical remodeling, autonomic remodeling, and ion-channel remodeling, lowers ventricular fibrosis, and suppresses depression-induced inflammatory responses, providing new insights in pinocembrin and ventricular arrhythmias in depressed patients.
Copyright © 2020 Ye, Zhang, Wu, Wan, Guo, Fo, Chen, Liu, Ran, Liang, Shi and Yang.

Entities:  

Keywords:  autonomic remodeling; depression; pinocembrin; ventricular electrical remodeling; ventricular fibrillation; ventricular fibrosis

Year:  2020        PMID: 33390936      PMCID: PMC7775674          DOI: 10.3389/fphar.2020.547966

Source DB:  PubMed          Journal:  Front Pharmacol        ISSN: 1663-9812            Impact factor:   5.810


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