Danqi soft caspule prevents atrial fibrillation by ameliorating left atrial remodeling through inhibiting cardiac fibroblasts differentiation and function

心房颤动 肌成纤维细胞 医学 纤维化 内科学 心室重构 心肌梗塞 心脏纤维化 心力衰竭 心功能曲线 心脏病学 内分泌学
作者
Jin Ma,Miao Ren,Jinxin Li,Chaoyang Zheng,Qiuxiong Chen,Salam Ma
出处
期刊:Phytomedicine [Elsevier]
卷期号:101: 154134-154134 被引量:3
标识
DOI:10.1016/j.phymed.2022.154134
摘要

Danqi soft capsule (DQ) is a Chinese herb medicine with a remarkable protective effect on cardio‐cerebrovascular diseases. The study aimed to investigate the role and mechanism of DQ on left atrial (LA) remodeling and atrial fibrillation (AF) occurrence in rats with post-myocardial infarction (MI) induced heart failure (HF). MI in rats was established by ligation of the left anterior descending coronary artery. DQ was administered to the post-MI induced HF rats over a 4-week period. AF inducibility was detected using the transesophageal programmed electrical stimulation technology. Echocardiogram, histology, and western blot analysis were performed. Meanwhile, cardiac fibroblasts (CFs) were performed to determine the effects of DQ on CFs function by 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT), flow cytometry, transwell assay and ELISA. The DQ-treated rats showed lower rates of AF inducibility and shorter AF durations than the MI rats. Moreover, DQ inhibited fibrosis and increased the expression of Cx43 in the left atrium; it also inhibited the myofibroblasts differentiation by reducing the expression of cytokines TNF-α, IL-6, and TGF-β1 via the TGF-β1/Smad 3 pathway. In addition, DQ inhibited the proliferation, migration, and collagen secretion of CFs in vitro. DQ reduces the risk of AF in post-MI HF rats by ameliorating LA arrhythmogenic substrate via inhibiting the function of proliferation, migration, collagen secretion, and myofibroblasts differentiation of CFs. Together, these results indicate the therapeutic potential of DQ in AF by delaying the progression of LA remodeling in post-MI-induced HF. Targeting CFs may be a novel prospective therapeutic avenue for AF after MI.
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