Administration with Yangxinshi ameliorates the progression of atrial fibrillation by affecting atrial remodeling and oxidative stress via the activation of the PI3K/AKT signaling

被引：0

作者：

Binmei Zhang ^{[1
]}

Jingxiu Hou ^{[2
]}

Li Dong ^{[1
]}

Man Sun ^{[3
]}

Ying Dong ^{[1
]}

Yumei Dong ^{[1
]}

机构：

[1] The Fourth Affiliated Hospital of Harbin Medical University,Department of Cardiology

[2] The First Affiliated Hospital of Chongqing Medical University,Department of Cardiology

[3] The Fourth Affiliated Hospital of Harbin Medical University,Department of Endocrinology

来源：

Cytotechnology | 2025年 / 77卷 / 3期

关键词：

Yangxinshi; Atrial fibrillation; Atrial remodeling; Oxidative stress; Network pharmacology;

D O I：

10.1007/s10616-025-00778-8

中图分类号：

学科分类号：

摘要：

Atrial fibrillation (AF) is a common cardiac arrhythmia and constitutes a great global health burden. Traditional Chinese medicine Yangxinshi exerts protective efficacy in cardiovascular diseases. However, its function in AF remains elusive. Here, Yangxinshi attenuated induction and duration of AF in acetylcholine (Ach)–CaCl2-constructed AF rat model, inducing inhibitory efficacy in susceptibility to AF. Moreover, Yangxinshi decreased AF-evoked atrial enlargement by inhibiting left atrial diameter (LAD) and LA area. Yangxinshi attenuated AF-induced oxidative stress by inhibiting elevation of ROS and 8-OHdG and ameliorated cell apoptosis in atria in AF rats. Moreover, Yangxinshi reduced atrial fibrosis levels, concomitant with decreases in collagen I, collagen III, and α-SMA. The network pharmacological analysis identified 110 common target genes between AF and Yangxinshi, and 6 major active ingredients of Yangxinshi that intersected with AF. GO and KEGG enrichment assay identified 20 pathways related to Yangxinshi targets in AF, among which the PI3K/AKT signaling had the greatest impact. Importantly, inactivation of the PI3K/AKT pathway in AF rats was offset by Yangxinshi. Together, Yangxinshi may attenuate the progression of AF by affecting atrial structural remodeling (atrial enlargement and fibrosis) and oxidative stress injury via the activation of the PI3K/AKT pathway, supporting a promising therapeutic agent for AF.

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