Shensong Yangxin capsule reduces atrial fibrillation susceptibility by inhibiting atrial fibrosis in rats with post-myocardial infarction heart failure

被引:23
|
作者
Ma, Jin [1 ]
Yin, Chunxia [1 ]
Ma, Shiyu [2 ]
Qiu, Huiliang [1 ]
Zheng, Chaoyang [1 ]
Chen, Qiuxiong [1 ]
Ding, Chunhua [1 ,3 ]
Lv, Weihui [1 ]
机构
[1] Guangzhou Univ Chinese Med, Affiliated Hosp 2, Heart Ctr, Guangdong Prov Hosp Chinese Med, 55 Neihuan Xilu, Guangzhou 510006, Guangdong, Peoples R China
[2] Guangzhou Univ Chinese Med, Affiliated Hosp 2, Dept Crit Care Med, Guangdong Prov Hosp Chinese Med, Guangzhou 510006, Guangdong, Peoples R China
[3] Peking Univ, Aerosp Ctr Hosp, Cardiac Dept, Aerosp Clin Coll Med, 15 Yuquan Rd, Beijing 100049, Peoples R China
来源
DRUG DESIGN DEVELOPMENT AND THERAPY | 2018年 / 12卷
关键词
Shensong Yangxin capsule; atrial fibrillation; fibrosis; electrophysiology; heart failure; MYOCARDIAL FIBROSIS; VULNERABLE SUBSTRATE; TISSUE INHIBITOR; MECHANISMS; PREVENTS; HOSPITALIZATIONS; DYSFUNCTION; EXPRESSION; INSIGHTS; BETA-1;
D O I
10.2147/DDDT.S182834
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Purpose: Shensong Yangxin (SSYX) capsule is a traditional Chinese medicine that has been used widely to treat cardiac arrhythmia. This study aimed to assess whether SSYX prevents atrial fibrillation (AF) after chronic myocardial infarction (MI)-induced heart failure and to determine the underlying mechanisms. Materials and methods: The study included 45 male Sprague Dawley rats. The rats underwent MI induction or sham surgery. One week after MI induction surgery, we performed serial echocardiography and administered SSYX capsule to some rats that experienced MI. After 4 weeks of treatment, AF inducibility was assessed with transesophageal programmed electrical stimulation technology. Additionally, multielectrode array assessment, histological analysis, and Western blot analysis were performed. Results: AF inducibility was significantly lower in SSYX rats than in MI rats (33.3% vs 73.3%, P<0.05). Additionally, conduction velocities in the left atrium were greater in SSYX rats than in MI rats. Moreover, SSYX decreased left atrial fibrosis, downregulated TGF-beta 1, MMP-9, TIMP-I, and type I and III collagen expressions, and inhibited the differentiation of cardiac fibroblasts to myofibroblasts. Conclusion: SSYX reduces AF inducibility after MI by improving left atrial conduction function via the inhibition of left atrial fibrosis. It prevents the development of an MI-induced vulnerable substrate for AF.
引用
收藏
页码:3407 / 3418
页数:12
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