Pinocembrin alleviates the susceptibility to atrial fibrillation in isoproterenol-induced rats

被引:5
作者
Liu, Zhangchi [1 ,2 ,3 ]
Chen, Xiaoli [1 ,2 ,3 ]
Ye, Tianxin [4 ]
Wan, Weiguo [1 ,2 ,3 ]
Yu, Yi [1 ,2 ,3 ]
Zhang, Cui [1 ,2 ,3 ,5 ]
Yang, Bo [1 ,2 ,3 ,5 ]
机构
[1] Wuhan Univ, Dept Cardiol, Renmin Hosp, Wuhan 430060, Peoples R China
[2] Wuhan Univ, Cardiovasc Res Inst, Wuhan 430060, Peoples R China
[3] Hubei Key Lab Cardiol, Wuhan 430060, Peoples R China
[4] Zhejiang Univ, Affiliated Hosp 1, Dept Cardiol, Sch Med, Hangzhou, Peoples R China
[5] Wuhan Univ, Dept Cardiol & Cardiovasc, Res Inst, Renmin Hosp, 238 jiefang Rd, Wuhan 430060, Hubei, Peoples R China
关键词
Isoproterenol; Atrial fibrillation; Atrial electrical remodeling; Inflammation; OXIDATIVE STRESS; INFLAMMATION; FIBROSIS; REFRACTORINESS; ARRHYTHMIAS; DYSFUNCTION; INHIBITION; CALCIUM; MARKERS;
D O I
10.1016/j.bbrc.2022.10.036
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: Inflammation can contribute to the initiation and progression of atrial fibrillation (AF), and pinocembrin can suppress downstream inflammatory cytokine production by inhibiting the inflammation pathway. In our previous studies, pinocembrin was also beneficial in ameliorating cardiac arrhythmia in different models of rats, such as depression, myocardial infarction, and heart failure. This study aims to investigate the effect of pinocembrin on the susceptibility to AF in isoproterenol-induced rats. Methods: Rats were randomly divided into four groups. Pinocembrin was injected through the tail vein. Isoproterenol was treated by intraperitoneal injection for one week (5 mg/kg/day). We evaluated the susceptibility to AF by atrial electrophysiological experiments. Masson staining was used to evaluate the fibrosis area. The protein levels of connexin (Cx) 40, Cav1.2, Kv4.2, collagen I, collagen III, a-SMA, transforming growth factor (TGF)-b, NLRP3, caspase 1, and interleukin (IL)-1b were detected by western blot. Results: Our data demonstrated that pinocembrin could prolong the atrial effective refractory period (ERP) and action potential duration (APD), and decrease AF inducibility. Isoproterenol increased the expression of Cav1.2 and Kv4.2 ion channels whereas pinocembrin could alleviate this change. Pinocembrin could reduce the fibrosis area, fibrosis-related protein collagen I, collagen III, a-SMA, and TGF-b and upregulate gap junction protein Cx40. In addition, pinocembrin reduced the expression of NLRP3, caspase 1, and IL-1b. Conclusions: Our study indicated that pinocembrin was beneficial to alleviate atrial electrical remodeling and fibrosis. Accompanied the downregulation of ion channels and upregulation of gap junction protein Cx40. Pinocembrin may produce these effects by inhibiting the NLRP3 pathway. (c) 2022 Elsevier Inc. All rights reserved.
引用
收藏
页码:33 / 40
页数:8
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