Key result
EGCG at 100 mg/kg/d significantly reduced the induction rate of Ang-II-induced atrial fibrillation compared to control (7.5% vs 61.1%, p<0.05) by inhibiting atrial fibrosis.
Why the study?
The study aimed to investigate the effect and mechanism of epigallocatechin-3-gallate on atrial fibrillation in rats.
Does EGCG reduce the occurrence and maintenance of atrial fibrillation in an Ang-II-induced rat model?
Does EGCG reduce the occurrence and maintenance of atrial fibrillation in an Ang-II-induced rat model?
EGCG attenuates Ang-II-induced atrial fibrosis and reduces the occurrence and duration of atrial fibrillation in rats by downregulating the TGF-β/Smad3 signaling pathway.
Purpose The aim of this study was to investigate the effect and mechanism of epigallocatechin-3-gallate (EGCG) on atrial fibrillation (AF) in rats. Methods A rat AF model was established by angiotensin-II (Ang-II) induction, 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 increasedsignificantly 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 TGF-βSmad3 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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Li et al. (2022) studied Atrial fibrillation and atrial fibrosis (n=109). Epigallocatechin-3-gallate (EGCG) vs. Ang-II alone was evaluated on Atrial fibrillation induction rate (p=<0.05). EGCG at 100 mg/kg/d significantly reduced the induction rate of Ang-II-induced atrial fibrillation compared to control (7.5% vs 61.1%, p<0.05) by inhibiting atrial fibrosis.
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