Epigallocatechin-3-Gallate Inhibits Atrial Fibrosis and Reduces the Occurrence and Maintenance of Atrial Fibrillation and its Possible Mechanisms.

IF 3.1 3区医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Cardiovascular Drugs and Therapy Pub Date : 2024-10-01 Epub Date: 2023-03-31 DOI:10.1007/s10557-023-07447-y

Tao Li, Qi Tong, Zhengjie Wang, Ziqi Yang, Yiren Sun, Jie Cai, Qiyue Xu, Yuan Lu, Xuemei Liu, Ke Lin, Yongjun Qian

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引用次数: 0

Abstract

Background: Atrial fibrosis is one of the main causes of the onset and recurrence of atrial fibrillation (AF), for which there is no effective treatment. The aim of this study was to investigate the effect and mechanism of epigallocatechin-3-gallate (EGCG) on AF in rats.

Methods: The rat model of AF was established by rapid pacing induction after angiotensin-II (Ang-II) induced atrial fibrosis to verify the relationship between atrial fibrosis and the AF. The expression levels of TGF-β/Smad3 pathway molecules and lysyl oxidase (LOX) in AF were detected. Subsequently, EGCG was used to intervene Ang-II-induced atrial fibrosis to explore the role of EGCG in the treatment of AF and its inhibitory mechanism on fibrosis. It was further verified that EGCG inhibited the production of collagen and the expression of LOX through the TGF-β/Smad3 pathway at the cellular level.

Results: The results showed that the induction rate and maintenance time of AF in rats increased with the increase of the degree of atrial fibrosis. Meanwhile, the expressions of Col I, Col III, molecules related to TGF-β/Smad3 pathway, and LOX increased significantly in the atrial tissues of rats in the Ang-II induced group. EGCG could reduce the occurrence and maintenance time of AF by inhibiting the degree of Ang-induced rat atrial fibrosis. Cell experiments confirmed that EGCG could reduce the synthesis of collagen and the expression of LOX in cardiac fibroblast induced by Ang-II. The possible mechanism is to down-regulate the expression of genes and proteins related to the TGF-β/Smad3 pathway.

Conclusion: EGCG could downregulate the expression levels of collagen and LOX by inhibiting the TGF-β/Smad3 signaling pathway, alleviating Ang-II-induced atrial fibrosis, which in turn inhibited the occurrence and curtailed the duration of AF.

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表没食子儿茶素-3-棓酸盐抑制心房纤维化并减少心房颤动的发生和维持及其可能机制

背景：心房纤维化是心房颤动（房颤）发病和复发的主要原因之一，目前尚无有效的治疗方法。本研究旨在探讨表没食子儿茶素-3-棓酸盐（EGCG）对大鼠房颤的影响和机制：方法：在血管紧张素Ⅱ（Ang-Ⅱ）诱导心房纤维化后，通过快速起搏诱导建立大鼠房颤模型，以验证心房纤维化与房颤之间的关系。检测了房颤中TGF-β/Smad3通路分子和赖氨酰氧化酶（LOX）的表达水平。随后，用EGCG干预Ang-II诱导的心房纤维化，以探讨EGCG在治疗房颤中的作用及其对纤维化的抑制机制。进一步验证了EGCG在细胞水平上通过TGF-β/Smad3途径抑制胶原蛋白的生成和LOX的表达：结果表明，大鼠房颤的诱发率和维持时间随心房纤维化程度的增加而增加。同时，Ang-II诱导组大鼠心房组织中Col I、Col III、TGF-β/Smad3通路相关分子和LOX的表达明显增加。EGCG可抑制Ang诱导的大鼠心房纤维化程度，从而减少房颤的发生和维持时间。细胞实验证实，EGCG能减少Ang-II诱导的心脏成纤维细胞中胶原蛋白的合成和LOX的表达。其可能的机制是下调与TGF-β/Smad3通路相关的基因和蛋白的表达：结论：EGCG可通过抑制TGF-β/Smad3信号通路下调胶原蛋白和LOX的表达水平，减轻Ang-II诱导的心房纤维化，从而抑制房颤的发生并缩短房颤持续时间。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cardiovascular Drugs and Therapy 医学-心血管系统

CiteScore

8.30

自引率

0.00%

发文量

110

审稿时长

4.5 months

期刊介绍： Designed to objectively cover the process of bench to bedside development of cardiovascular drug, device and cell therapy, and to bring you the information you need most in a timely and useful format, Cardiovascular Drugs and Therapy takes a fresh and energetic look at advances in this dynamic field. Homing in on the most exciting work being done on new therapeutic agents, Cardiovascular Drugs and Therapy focusses on developments in atherosclerosis, hyperlipidemia, diabetes, ischemic syndromes and arrhythmias. The Journal is an authoritative source of current and relevant information that is indispensable for basic and clinical investigators aiming for novel, breakthrough research as well as for cardiologists seeking to best serve their patients. Providing you with a single, concise reference tool acknowledged to be among the finest in the world, Cardiovascular Drugs and Therapy is listed in Web of Science and PubMed/Medline among other abstracting and indexing services. The regular articles and frequent special topical issues equip you with an up-to-date source defined by the need for accurate information on an ever-evolving field. Cardiovascular Drugs and Therapy is a careful and accurate guide through the maze of new products and therapies which furnishes you with the details on cardiovascular pharmacology that you will refer to time and time again.