Pinocembrin attenuates autonomic dysfunction and atrial fibrillation susceptibility via inhibition of the NF-κB/TNF-α pathway in a rat model of myocardial infarction
•Pinocembrin decreased myocardial infarction (MI)-induced autonomic remodeling.•Pinocembrin ameliorated MI-induced atrial electrical remodeling.•Pinocembrin decreased MI-induced atrial fibrosis.•Pinocembrin decreased atrial fibrillation susceptibility in MI rats.•Pinocembrin suppressed MI-induced in...
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Published in | International immunopharmacology Vol. 77; p. 105926 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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01.12.2019
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Abstract | •Pinocembrin decreased myocardial infarction (MI)-induced autonomic remodeling.•Pinocembrin ameliorated MI-induced atrial electrical remodeling.•Pinocembrin decreased MI-induced atrial fibrosis.•Pinocembrin decreased atrial fibrillation susceptibility in MI rats.•Pinocembrin suppressed MI-induced inflammatory responses.
Previous studies indicate that myocardial infarction (MI) may contribute to atrial fibrillation (AF). Emerging evidence has shown that pinocembrin protects myocardial ischemic injury (I/R)-induced cardiac fibrosis and arrhythmias in animals via its anti-inflammatory or antioxidant activities. However, the effects of pinocembrin on MI-induced atrial arrhythmias remain unknown. Thus, this study aimed to investigate the effects of pinocembrin on autonomic dysfunction and AF susceptibility in MI rats and the possible mechanism. In a standard experimental MI model, Sprague-Dawley rats received permanent ligation of the left anterior descending (LAD) coronary artery and were treated with pinocembrin or saline for 6 days. Our results demonstrated that pinocembrin treatment significantly decreased sympathetic activity, augmented parasympathetic activity, improved heart rate variability (HRV), prolonged the atrial effective refractory period (ERP) and action potential duration (APD), shortened activation latency (AL), lowered the indicibility rate of AF, attenuated atrial fibrosis, and decreased concentrations of norepinephrine (NE), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in the serum and the left atrial (LA). Furthermore, pinocembrin treatment significantly increased the expression levels of Cx43 and Cav1.2 and suppressed the phosphorylation of inhibitor-κBα (IκBα) and the activation of nuclear factor-kappa B (NF-κB)subunit p65. In conclusion, the findings indicate that pinocembrin treatment decreases autonomic remodeling, lowers atrial fibrosis, ameliorates atrial electrical remodeling, and suppresses MI-induced inflammatory responses, which suggests a potential novel strategy for atrial arrhythmias. |
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AbstractList | Previous studies indicate that myocardial infarction (MI) may contribute to atrial fibrillation (AF). Emerging evidence has shown that pinocembrin protects myocardial ischemic injury (I/R)-induced cardiac fibrosis and arrhythmias in animals via its anti-inflammatory or antioxidant activities. However, the effects of pinocembrin on MI-induced atrial arrhythmias remain unknown. Thus, this study aimed to investigate the effects of pinocembrin on autonomic dysfunction and AF susceptibility in MI rats and the possible mechanism. In a standard experimental MI model, Sprague-Dawley rats received permanent ligation of the left anterior descending (LAD) coronary artery and were treated with pinocembrin or saline for 6 days. Our results demonstrated that pinocembrin treatment significantly decreased sympathetic activity, augmented parasympathetic activity, improved heart rate variability (HRV), prolonged the atrial effective refractory period (ERP) and action potential duration (APD), shortened activation latency (AL), lowered the indicibility rate of AF, attenuated atrial fibrosis, and decreased concentrations of norepinephrine (NE), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in the serum and the left atrial (LA). Furthermore, pinocembrin treatment significantly increased the expression levels of Cx43 and Cav1.2 and suppressed the phosphorylation of inhibitor-κBα (IκBα) and the activation of nuclear factor-kappa B (NF-κB)subunit p65. In conclusion, the findings indicate that pinocembrin treatment decreases autonomic remodeling, lowers atrial fibrosis, ameliorates atrial electrical remodeling, and suppresses MI-induced inflammatory responses, which suggests a potential novel strategy for atrial arrhythmias. •Pinocembrin decreased myocardial infarction (MI)-induced autonomic remodeling.•Pinocembrin ameliorated MI-induced atrial electrical remodeling.•Pinocembrin decreased MI-induced atrial fibrosis.•Pinocembrin decreased atrial fibrillation susceptibility in MI rats.•Pinocembrin suppressed MI-induced inflammatory responses. Previous studies indicate that myocardial infarction (MI) may contribute to atrial fibrillation (AF). Emerging evidence has shown that pinocembrin protects myocardial ischemic injury (I/R)-induced cardiac fibrosis and arrhythmias in animals via its anti-inflammatory or antioxidant activities. However, the effects of pinocembrin on MI-induced atrial arrhythmias remain unknown. Thus, this study aimed to investigate the effects of pinocembrin on autonomic dysfunction and AF susceptibility in MI rats and the possible mechanism. In a standard experimental MI model, Sprague-Dawley rats received permanent ligation of the left anterior descending (LAD) coronary artery and were treated with pinocembrin or saline for 6 days. Our results demonstrated that pinocembrin treatment significantly decreased sympathetic activity, augmented parasympathetic activity, improved heart rate variability (HRV), prolonged the atrial effective refractory period (ERP) and action potential duration (APD), shortened activation latency (AL), lowered the indicibility rate of AF, attenuated atrial fibrosis, and decreased concentrations of norepinephrine (NE), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in the serum and the left atrial (LA). Furthermore, pinocembrin treatment significantly increased the expression levels of Cx43 and Cav1.2 and suppressed the phosphorylation of inhibitor-κBα (IκBα) and the activation of nuclear factor-kappa B (NF-κB)subunit p65. In conclusion, the findings indicate that pinocembrin treatment decreases autonomic remodeling, lowers atrial fibrosis, ameliorates atrial electrical remodeling, and suppresses MI-induced inflammatory responses, which suggests a potential novel strategy for atrial arrhythmias. |
ArticleNumber | 105926 |
Author | Liu, Dishiwen Yang, Bo Zhang, Cui Wan, Weiguo Liang, Jinjun Liu, Xin Ye, Tianxin Wu, Gang |
Author_xml | – sequence: 1 givenname: Tianxin surname: Ye fullname: Ye, Tianxin – sequence: 2 givenname: Cui surname: Zhang fullname: Zhang, Cui – sequence: 3 givenname: Gang surname: Wu fullname: Wu, Gang – sequence: 4 givenname: Weiguo surname: Wan fullname: Wan, Weiguo – sequence: 5 givenname: Jinjun surname: Liang fullname: Liang, Jinjun – sequence: 6 givenname: Xin surname: Liu fullname: Liu, Xin – sequence: 7 givenname: Dishiwen surname: Liu fullname: Liu, Dishiwen – sequence: 8 givenname: Bo surname: Yang fullname: Yang, Bo email: yybb112@whu.edu.cn |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31704291$$D View this record in MEDLINE/PubMed |
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Keywords | Myocardial infarction Autonomic remodeling Inflammatory response Pinocembrin Atrial fibrillation |
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Snippet | •Pinocembrin decreased myocardial infarction (MI)-induced autonomic remodeling.•Pinocembrin ameliorated MI-induced atrial electrical remodeling.•Pinocembrin... Previous studies indicate that myocardial infarction (MI) may contribute to atrial fibrillation (AF). Emerging evidence has shown that pinocembrin protects... |
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SubjectTerms | Action potential Activation Animals Antioxidants Atrial fibrillation Atrial Fibrillation - drug therapy Atrial Fibrillation - metabolism Atrial Fibrillation - physiopathology Autonomic remodeling Calcium channels (voltage-gated) Calcium Channels, L-Type - metabolism Cardiac arrhythmia Cardiotonic Agents - pharmacology Cardiotonic Agents - therapeutic use Connexin 43 Connexin 43 - metabolism Coronary artery Cytokines - metabolism Dysautonomia Electrocardiography Fibrillation Fibrosis Flavanones - pharmacology Flavanones - therapeutic use Heart Atria - drug effects Heart Atria - physiopathology Heart attacks Heart rate Heart Rate - drug effects Inflammation Inflammatory response Interleukin 6 Ischemia Latency Male Myocardial infarction Myocardial Infarction - drug therapy Myocardial Infarction - metabolism Myocardial Infarction - physiopathology NF-KappaB Inhibitor alpha - metabolism NF-κB protein Norepinephrine Parasympathetic nervous system Phosphorylation Pinocembrin Rats, Sprague-Dawley Refractory period Transcription Factor RelA - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α |
Title | Pinocembrin attenuates autonomic dysfunction and atrial fibrillation susceptibility via inhibition of the NF-κB/TNF-α pathway in a rat model of myocardial infarction |
URI | https://dx.doi.org/10.1016/j.intimp.2019.105926 https://www.ncbi.nlm.nih.gov/pubmed/31704291 https://www.proquest.com/docview/2330967734 https://search.proquest.com/docview/2313358134 |
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